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You are an expert translator fluent in English and Traditional Chinese. Your task is to perform a context-aware, paragraph-by-paragraph translation from English to Traditional Chinese, producing text that reads naturally to a native speaker.
Step 1: Read and Analyze
Carefully read the entire text before translating. Identify the tone, style, target audience, and overall message. If necessary, infer any cultural or thematic elements that may influence the translation.
Step 2: Summary (in English)
Briefly summarize the overall meaning and tone of the text to demonstrate your understanding of its context and nuance.
Step 3: Natural and Cohesive Translation
Translate the text paragraph by paragraph, focusing on the following:
Ensure accuracy of meaning, not literal structure.
Adapt idioms, metaphors, and nuanced expressions for a Traditional Chinese-speaking audience.
Prioritize fluency: the translation should sound like it was originally written in Traditional Chinese, not translated.
Rephrase or reorder sentences if necessary to improve readability and natural flow.
Maintain the tone and style appropriate to the original.
Each paragraph is separated by the \n character.
Use the following format for output in full compiled translation:
[Paragraph translated into Traditional Chinese]
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THE LOW-CARB FRAUD
It’s no secret that Americans struggle with weight loss. Since 1980, when the rise in obesity first caught the attention of the media, the national rate of obesity has doubled.1 Now, more than one-third of all U.S. adults are obese. And despite hundreds of new (or cleverly recycled) “solutions” hitting the shelves in book or prepackaged food form each year, we just can’t seem to stem the tide. Our national weight problem is just the tip of the iceberg, however; being overweight is linked to some of the major causes of premature death, including heart disease, stroke, Type 2 diabetes, and some cancers.2
This book is primarily about low-carb diets—one of the more financially successful, and one of the most health-threatening, solutions proposed to meet our desire to shed pounds and become healthier. We’ll discuss why the low-carb diet is so appealing, how we’ve been tricked in thinking it’s healthy, and the truth about its health impacts. But this book is also concerned with the beliefs about nutrition that underlie those things: where the belief that carbs are bad came from, and why it has persisted despite so much evidence to the contrary.
There have almost always been fad diets with varying degrees of scientific merit, some more effective than others. Several decades ago, and still to a certain extent today, the most trusted advice was, essentially: eat less and exercise more. Weight loss was a matter of arithmetic—calories in vs. calories out. But we were also told that dietary fat is the problem. Fat is what makes us, well, fat. So if we want to lose weight, all we have to do is consume less of it.
But as the national obesity rate rose, it was clear that this advice on fat just wasn’t cutting it. The Standard American Diet (SAD) also wasn’t cutting it. We needed to rethink the way we looked at proper nutrition. It was during the 1980s, in the wake of these rising concerns, that the low-carb movement began to take hold. It hit its stride in 1988, with the publication of Dr. Robert Atkins’ New Diet Revolution, which was “new” only in that it followed Atkins’ 1972 book, Dr. Atkins’ Diet Revolution, which had not been especially successful in the marketplace. And this “new” book’s contents represented an appealing alternate belief system about weight, nutrition, and health.
In a nutshell, the low-carb movement told adherents to severely limit their intake of carbohydrates and instead to get the lion’s share of their calories from protein and fat. The problem with the SAD isn’t fat, the book claims, but carbs—those found in bread, rice, and pasta, in fruit and starchy vegetables. The best way to lose weight, Atkins proclaims, is to cut back on carbs.
And it worked! By feasting on bacon and steak and butter, low-carb dieters actually did drop pounds. Which would be great, except for one important thing: the low-carb diet is not good for human health. Report after report has shown the ill effects of a high-protein, high-fat diet. It’s just as bad, if not worse, than the SAD it seeks to replace.
In this book, I will explore a couple of important questions: Why do people think low-carb diets are a good idea? What’s the truth behind the low-carb hype? What’s the truly optimal diet for achieving an ideal weight while also obtaining health and longevity?
If there’s one thing I hope you’ll take away from this book, it’s this: the low-carb diet’s ability to bring about quick weight loss is far outweighed by the serious health problems that accompany such an animal foods–heavy diet.
THE LOW-CARB APPEAL
I’ve spent more than forty years in experimental nutritional research, first at Virginia Tech and then at Cornell, keeping up with the latest discoveries and doing my own work, both in the lab and in the field. And as a nutritional researcher, I was surprised at first by the popularity and commercial success of the low-carb diet, especially given its serious flaws. The research on high-protein, high-fat diets has consistently demonstrated that they have disastrous health effects and fail to secure compliance and long-term weight loss. So I think it’s useful to point out some factors that have contributed to these diets’ appeal.
It’s easy to imagine why dieters might be swayed—both then and now—by the idea of trying something radically different. Millions of Americans are on diets. Food manufacturers and marketers flood the marketplace with foods designed to help us lose weight and keep it off. Television features a steady stream of infomercials touting new gadgets, exercise routines, pills, and powders that can help us shed those unsightly pounds. And, apparently, none of it is working.
For a shocking visual, compare these two slides, taken from a CDC presentation. The first slide shows data from 1990 and is far from ideal:
Forty-six of the fifty-two states and other U.S. jurisdictions report adult obesity rates between 10 and 20 percent, with obesity defined as a Body Mass Index (BMI) greater than 30. No state has an obesity rate above 20 percent.
Now look at the data from 2010:
Just twenty years later, the thinnest states—with obesity rates under 25 percent—are all heavier than the heaviest states in 1990. And twelve states have cracked the 30-percent-plus mark.
The 2011 data, which haven’t made it into the slideshow yet, include a new category: 35 percent or greater adult obesity rate. While it wasn’t strictly necessary to add that category (Alabama came closest, with a 34.9 percent rate), the CDC were obviously planning ahead.3
Given the huge diet industry and its stunning lack of effectiveness, it’s only natural that alternative approaches would gain popularity. Low-carb was the alternative that gained the largest amount of public acceptance and hence the greatest market share. But why did low-carb beat out the other nontraditional approaches?
One of the main answers is marketing rhetoric. On this point, I have to take my hat off to Robert Atkins. One of the major themes of my new book on nutritional science, Whole: Rethinking the Science of Nutrition (2013), is that paradigms, or entrenched ways of seeing the world, are devilishly hard to change. But Atkins and his supporters turned a century of nutritional wisdom on its head, framing dietary fat and cholesterol as nutritional heroes and attacking anyone who pointed to research showing otherwise. They gave Americans permission to eat huge amounts of some of the unhealthiest foods on the planet, and to do so not only without guilt, but with feelings of pride and superiority. The most impressive legacy of the Atkins craze is a linguistic achievement: coining the phrase “low-carb” and thereby turning most plant foods—which were previously considered the healthiest dietary choices—into dangerous and fattening no-nos.
The appeal of this was immediate, for obvious reasons. After decades of believing that losing weight was possible only by subsisting on salads, depressing lunches of grapefruit halves and fat-free cottage cheese, and diet sodas that taste like battery acid, people were told to eat as much as they wanted of their favorite foods: steak, bacon, butter, lard, cream cheese, olive oil, mayonnaise, and eggs. Eating was fun again!
And lo and behold, people found that—in the initial stages of this diet—they did lose weight. It seemed like the very foods that doctors and public officials had been warning against all those years actually promoted weight loss more effectively than the tasteless zero-fat processed foods that took all the joy from eating.
Not only could the Atkins followers sate their fat- and protein-cravings without guilt, they could even feel superior to the poor fools who were still eating salads, going to weight-loss meetings, and counting calories.
The Atkins Diet didn’t just appeal to dieters; it was a boon to the meat, dairy, and egg industries as well. Not only could these companies now fend off public criticism of their products with low-carb “science,” but they also saw greater sales.
THE LOW-CARB LANDSCAPE
Not all low-carb diets are created equal, of course. The low-carb universe Atkins brought into being has grown to encompass many different diets and eating philosophies. But these are distinguished more by marketing than by substance—they all share the same fear and loathing of carbohydrates and recommend getting most of one’s calories from protein and fat.
Atkins
While Robert Atkins is the father of the modern low-carb movement, he didn’t come up with the low-carb concept, something he freely admits in his books. The first person on record as having used this type of diet was William Banting, a British undertaker, in the 1860s. Banting, at the age of sixty-six, tried a low-carb diet at the recommendation of his physician, Dr. William Harvey. He lost body weight in the first few weeks and commented that he might like to continue the diet—though the longer-term results of Banting’s alteration in diet, to my knowledge, were never clear. A few other medical practitioners experimented with low-carb diets with their patients over the next century, but the idea didn’t enter mass public consciousness until the 1972 publication of Dr. Atkins’ Diet Revolution.
Riding the wave of the low-carb diet’s near-term success, Atkins authored many additional books before his passing in 2003. His professional career morphed into an empire; as of this writing in 2013, the 1988 Dr. Atkins’ New Diet Revolution has sold more than 15 million copies, and Atkins Nutritionals, Inc., which produces and licenses Atkins-approved products, achieves annual sales in the millions of dollars. The Atkins Foundation funds research on the low-carb diet as it relates to obesity, Alzheimer’s, prostate cancer, and other diseases. And the Atkins empire perseveres, despite its founder’s death and a descent into bankruptcy following company mismanagement in 2004–2005; its present-day business still claims a big piece of the weight-loss market.
Low-Carb Spinoffs
Smelling profits, many other doctors and authors put their own spin on the low-carb phenomenon and created their own books, diets, and products. Most prominent among them are Mary Dan and Michael Eades’ Protein Power (1995), Barry Sears’ Enter the Zone (1995), Peter D’Adamo’s Eat Right 4 Your Type (1997), Loren Cordain’s The Paleo Diet (2002), Arthur Agatson’s South Beach Diet (2005), and Eric Westman’s The New Atkins for a New You (2010). Like younger siblings struggling to stand out, these various authors and their supporters go to great lengths to distinguish their “correct” diet from the others. The South Beach Diet prefers olive oil to butter and emphasizes leaner cuts of meat. Protein Power adds lots of water and nutritional supplementation to compensate for the low-carb diet’s inadequacies. Enter the Zone seemingly dismisses the low-carb idea by recommending “only” 30 percent protein but still relegates carbs to less than half your total calories. (That’s still low carb!) Even The Paleo Diet, despite its positive emphasis on whole foods, is just another version of the same low-carb, high-protein, high-fat idea (see Appendix). These spinoffs all occupy the same very thin slice of the human diet continuum.
In addition to their carbophobia, these authors have two other things in common: no experience in scientific research and a vast fortune generated by the sales of their shakes, powders, extracts, oils, bars, and even chocolates, along with a second fortune amassed through licensing their trademarked seal of approval.
The net effect of all this differentiation and marketing has been the normalization of low carb on a cultural level. Restaurants routinely offer low-carb menu options. It’s expected that someone watching their weight will bypass the dinner rolls. And whereas twenty years ago you would have raised an eyebrow (and a few concerns for your sanity) were you to sit down to a meal of bacon, butter, and beef for the purpose of shedding pounds, these days that’s a perfectly normal approach to weight loss. When absurdities get repeated often enough, they start sounding like truth.
THE REAL TRUTH ABOUT LOW-CARB DIETS
As I mentioned, low-carb diets are often pretty good at bringing about short-term weight loss. But that benefit comes with huge downsides. Low-carb diets target excess weight without paying attention to the underlying cause or causes of that weight, which leads to other symptoms. Low-carb diets often make those other symptoms, as well as the cause itself, worse.
What’s the difference between attending to a cause and treating a symptom?
A brown lawn, for example, is a symptom. It’s an unsightly, possibly embarrassing symptom that could get your neighbors shaking their heads and talking about you behind your back. “Look how he lets his lawn go,” they might mutter. “Why doesn’t he do something about it?”
So along comes the lawn-care specialist with a solution to your problem: green paint.
Voilà—problem solved!
Well, not exactly.
After painting the grass, your lawn will look green temporarily, but eventually the paint will wear or wash away, and then you have to call the lawn painter back in. The paint doesn’t do anything about the poor health of the grass that led to it turning brown in the first place. And if the paint is toxic, it can even make the health of the grass worse. If you really want a lush green lawn—a healthy lawn that is naturally green—you need to improve the soil: add nutrients, remove toxins, water appropriately, and use the right grass seed for your environment. In other words, focus on the root causes, not just the visible symptoms.
If you want to lose weight, focusing solely on weight loss—as the low-carb diet does—is as unproductive as painting your lawn green.
The low-carb diet’s first major flaw is that it’s short term. Over the long term, low-carb diets don’t fulfill their promise to dieters, which is that the diet will help them reduce their weight and sustain the change. Observation studies of populations overwhelmingly show that high-protein, high-fat diets, which reflect the long-term consumption of animal-based and highly processed food products, are associated with more health problems, many of which are associated with obesity.4
Americans are getting heavier and sicker, despite all the modern advances in medical care and technology. We’re making no significant inroads in reducing rates of cancer, heart disease, stroke, diabetes, and dozens of other diseases intimately connected with obesity. It’s just that, unlike diabetes or high blood pressure, obesity is a more visible symbol of the problem.
In truth, the obesity epidemic and the health crisis are two sides of the same coin. You can’t solve one without solving the other. That’s as true on an individual basis as it is for society as a whole. Obesity is a symptom, just like hypertension, clogged arteries, angina, chronic shortness of breath, belly pain, dizziness, constipation, and hundreds of others. Yet we largely, and wrongly, treat obesity as if it’s a separate thing—a separate disease.
While there’s a lot of overlap between a healthy body weight and overall health, they aren’t synonymous. You can lose a lot of weight by getting cancer, and you can keep it off by dying, but I don’t recommend that approach! Charitably, we could say that low-carb advocates are using weight loss as a Trojan Horse to get people to improve their diets and overall health—although there’s little evidence for this generous interpretation. As Atkins himself was both obese and quite ill from the known consequences of a high-protein, high-fat diet at the time of his death,5 it’s clear that this community isn’t taking seriously the damning data on long-term health outcomes.
Two original research papers reveal more about the consequences of the Atkins Diet than any others because they were published by supporters of the Atkins Diet and were funded by the Atkins organization. In one paper,6 users of the Atkins diet, when compared to control subjects of “low-fat” dieters (dieters who were getting “only” 30 percent of their calories from fat), suffered more constipation (68 vs. 35 percent), more headaches (60 vs. 40 percent), more halitosis (38 vs. 8 percent), more muscle cramps (35 vs. 7 percent), more diarrhea (23 vs. 7 percent), more general weakness (25 vs. 8 percent), and more rashes (13 vs. 0 percent)—even those Atkins diet users who were taking vitamin supplements. In the other paper,7 similar prevalences were seen for the Atkins dieters for constipation (63 percent), headaches (53 percent), and halitosis (51 percent).
These Atkins Diet side effects are consistent, and the research is quite convincing. That is, when compared with the already poor Standard American Diet (SAD), which is high in fat and protein, the Atkins Diet, even higher in fat and protein, leads to far more negative health outcomes, even in the short term.
So why do dieters still believe the low-carb hype? It has a lot to do with how convincing the low-carb movement’s arguments sound—even though those arguments are consistently contradicted by the science.
GARY TAUBES AND LOW-CARB SLEIGHT OF HAND
The best lies contain a kernel of truth, and that’s certainly the case with the work of journalist Gary Taubes, by far the most eloquent and influential present-day spokesperson for the low-carb movement. Taubes’ two bestselling books, Good Calories, Bad Calories (2007) and Why We Get Fat (2011), make the low-carb case in an entertaining and, to many, compelling fashion.
Taubes is not, of course, the only person who writes in support of the low-carb diet, but I’ve chosen to center my critique around Taubes’ writings because they represent the most comprehensive and evidence-rich expression of the low-carb idea. Taubes’ work also provides—inadvertently, no doubt—a survey of many of the errors, logical problems, and sleights of hand common to low-carb advocates. By pointing out Taubes’ errors and exposing his faulty reasoning, I hope to show the failures and intellectual poverty of the entire low-carb movement.
The first and perhaps most damning problem is the misreading of history and of the supposed link between low-fat diets and obesity. Taubes tackles this history in Good Calories, Bad Calories, a book billed as required reading for those interested in the evidence supporting a low-carb diet. While Taubes’ account is certainly comprehensive, his interpretation is, shall we say, creative.
WHERE TAUBES GETS IT RIGHT
Taubes begins with a kernel of truth, rightly pointing out that the effectiveness of counting calories is a myth. He also gets right some of the important history of the narrative on diet and health of the past five decades. And in his technical arguments on the underlying biochemistry of obesity, he gets some of these details right as well. But considered in isolation and spun into a narrative about the evils of carbs, these partial truths end up misleading rather than informing.
Taubes correctly points out that many early researchers, in the way they crafted their studies and reported their findings, were confusing the three main hypotheses for the causes of obesity and related illnesses: excess calories, excess fat, and excess carbs. According to the first hypothesis—by far the most common—we gain weight because we ingest more calories than we burn. This is the hypothesis I mentioned earlier, which you still hear being invoked today as if it’s the most obvious thing in the world: “eat less, exercise more.” Simple arithmetic. To his credit, Taubes does a masterful job of debunking this dangerous oversimplification.
Taubes goes on to argue, correctly, that creating long-term health by controlling calorie consumption does not work—a very important observation little understood by professionals and nonprofessionals alike. Most people cannot maintain significantly lower calorie consumption for long periods of time, even though they may be able to do so for a short while. That is, “diets” don’t work—not because our willpower isn’t up to it but because of our biological inability to healthfully maintain the substantially lower calorie consumption required to significantly decrease disease formation.8 In any case, Taubes says, generally it is not the amount of calories consumed that matters most but the way calories are metabolized and distributed throughout the body (something we’ll discuss in more depth in a few pages). In fact, Taubes argues that increased calorie consumption is the effect, not the cause of obesity—that we gain weight for other reasons and then require more calories to sustain that weight. Something else is causing obesity, and it is doing so by determining how our ingested calories are metabolized and used.
I applaud Taubes’ demolishing the calorie hypothesis. In fact, I have long said that we should be careful not to emphasize the “calories in; calories out” hypothesis or describe calories in precise quantities as if they are physical entities, like molecules, that have structure and form, because doing so only gives them added importance.
A calorie is only a measure of energy contained within a molecule, especially within the chemical bonds that bind atoms. Think of a pile of wood. We know that there is energy in that pile of wood, but we cannot see or feel it. When we put a match to the wood, however, we feel that energy escaping as the wood bursts into flames. The calorie contents of nutrients are also determined by measuring the heat nutrients release when burned. To calculate this, macronutrients (fat, protein, and carbohydrates, the nutrients that provide the vast majority of the weight of food) are burned in controlled conditions in a laboratory, and the heat emitted—the temperature change—is measured as calories. (I prefer to call this property “energy” but will stick with “calories” here because of the term’s broad familiarity.)
The amount of calories needed to produce a noticeable change in body weight, up or down, is very small—a notion that also sidetracks our emphasis on calories. A difference of fifty calories can be difficult to distinguish in the context of a day’s total food intake; it’s equivalent to an average of less than a teaspoon of oil per day. Yet a difference of fifty calories retained by the body per day can theoretically cause a gain or loss of five to ten pounds of body weight per year.9 The problem is that consumption of calories does not equal retention of calories; retention of calories is not something we can consciously control by counting. So, in this respect, Taubes is correct: calorie intake or expenditure, except in the extreme, does not matter as our findings in China confirm.10
WHERE TAUBES GETS IT WRONG
Taubes parts company with the evidence when he gets into the identification of where “bad calories” come from. Taubes sees excess consumption of calorie-contributing carbohydrates (the second of the three competing theories mentioned previously) as the root of all dietary evil. In his view, the consumption of sugar (table sugar or sucrose) and other carbohydrates (i.e., refined carbohydrates, such as starch and fructose) is responsible for the obesity epidemic in the United States and much of the rest of the world. And he blames this spike in carbohydrate consumption on the government’s promotion of the third competing theory: that calories from fat make us fat. In Taubes’ view, the fear of fat engendered by government low-fat policies drove the American public straight into the arms of a high-carb diet because it encouraged the replacement of this fat with carbohydrates. In short, Taubes says that too many carbs is the problem, while the government (or his interpretation of it) says the problem is too much fat.
Taubes argues on historical and scientific grounds that excess fat consumption cannot account for the alarming rise in obesity during the past thirty years the way government pronouncements suggest. Most readers will be familiar with the widespread recommendation to use low-fat foods, as well as the multitudes of “low-fat” food products on the market. Taubes presents a seemingly plausible account of how scientists working in this field got it wrong, partly because they were not very imaginative and partly because they became entrenched in a worldview that discouraged professional challenge against the much-publicized low-fat-focused hypothesis lest they be ridiculed or even risk losing their professional standing. Fat, not carbohydrates, Taubes says, should be our primary source of energy. Fat is good, he says, and not something merely dumped into a body reservoir that eventually becomes adipose tissue.
Before going further, let’s consider what a carbohydrate actually is, especially because Taubes rather arrogantly lambasts scientists for not knowing the properties of this nutrient. (In my experience, it’s really journalists like Taubes, corporate marketing agents, and even some clinicians who are confused about carbohydrates’ definition and meaning.)
The Diversity of Carbohydrates
Carbohydrate is a nutrient found almost exclusively in plants. It is a collection of simple to very complex chemical molecules. Simple carbohydrates include monosaccharides (like glucose, fructose, galactose, mannose, etc.) and disaccharides, which are made up of two chemically bonded monosaccharides (like sucrose [table sugar, made from glucose and fructose] and lactose [milk sugar, made from glucose and galactose]). Linked chains, or polymers, of three or more monosaccharides are called polysaccharides. Glucose (the same molecule as in blood sugar) is the most common monosaccharide unit in polysaccharide chains, with fructose being nearly as common in some foods. Starch, which is the primary polysaccharide in foods like potatoes and cereal grains, is a network of long chains of glucose molecules.
Monosaccharides and disaccharides are often considered “simple” carbohydrates because their molecular size is small, they readily dissolve in water, and they are easily digested and absorbed into the bloodstream. Some people infer that starches are also “simple” because they, too, dissolve in water (though they turn it into a gel or paste) and are readily broken down during digestion into glucose, which is then absorbed into the bloodstream.
Other carbohydrate types are much more complex. Elaborate networks of polymers are formed from chains of monosaccharides, sometimes also including amino acid and fat-like molecular side chains. These polymer networks exhibit a wide variety of chemical, physical, and nutritional properties. A large group of substances generally referred to as the dietary fiber group, for example, are, unlike their simple carbohydrate cousins, generally not digested and absorbed in the gut. Nonetheless, these complex, fiber-like substances still participate in vitally important biological activities: they interact with intestinal microorganisms that break them down into products that benefit the rest of the body, especially the intestines. Indeed, simple and complex carbohydrates, when working together, provide diverse health benefits, including the provision of energy.
Whenever we encounter diversity in nature, we should be slow to dismiss it as unnecessary or unfortunate. A broad spectrum of carbohydrate digestibility and function is very important: it allows the body to adapt to different conditions, ranging from the need for a quick burst of energy to the facilitation of digestion and absorption of other nutrients in the gut.
It’s true that sucrose, the simple disaccharide that comprises table sugar, can be harmful when consumed in isolation. Sucrose is known to have little or no useful health value when extracted from sugar cane and sugar beet plants and added in isolated form to other foods. High-fructose corn syrup is another simple monosaccharide of more recent commercial vintage and exploitation. The latest studies suggest that its effects are as bad as those of sucrose,11 if not worse.12
In order to use this evidence in support of the low-carb movement, Taubes performs a bit of sleight of hand, the crux of which is: refined sugar is bad, therefore all foods that contain sugars (i.e., carbs) are bad. This is poor logic even in the classical sense. We can also highlight the flaws in this reasoning by considering another carbohydrate found in plant food—fiber—and comparing its health effects when in its natural state and when processed, isolated, and consumed as a substance separate from that natural state.
Dietary fiber is extracted from all kinds of whole plants in order to add it to muffins and other baked goods as “bran.” Marketers then claim health benefits from these baked goods, citing the research evidence on the goodness of fiber. But bran doesn’t help us when it’s been extracted from whole plants and then stuck into processed and fragmented foods like breads and breakfast cereals. Although there is some evidence that bran supplements may reduce certain indicators of serious health problems, I find no evidence that, over the long term, this is a good option for actually preventing or treating these problems.13
Whole foods that contain dietary fiber, in its many complex forms, are associated with lower incidence of colon cancer, lower blood cholesterol, and lower breast cancer–inducing estrogen levels. The use of bran isolated from these foods is more about marketing than health. This holds true for many isolated nutrients, which either have no positive health benefits or actually result in damaging effects.
If Taubes and his low-carb compatriots are against ingesting refined (i.e., extracted) sugars, they should say so, and I’d be among the first to support their crusade to eliminate those sugars from our diets. But instead, they tar the entire class of carbohydrates with the same brush, which is an intellectually superficial and dishonest move. (Taubes is more careful than some other low-carb cheerleaders, but not completely so. He should be proactively emphasizing this discrepancy, not allowing it to smolder just below the public narrative.)
Because fruits, vegetables, and whole grains are all high in carbohydrates, lumping all carbs together as unhealthy means demonizing plant-based foods as well as simple sugars. A diet low in carbohydrates is unavoidably a diet high in fat, especially saturated fat, because eliminating carbohydrates means relying on large quantities of animal-based products for energy and other nutritional benefits. Virtually by definition, therefore, a low-carb diet emphasizes the consumption of animal-based foods, while a low-fat diet emphasizes the consumption of plant-based foods. In my experience, it is this emphasis given to animal-based foods in low-carb (and thus high-protein, high-fat) diets that is the chief motivation of low-carb advocates.
The dramatic shift in consumption suggested by Taubes’ oversimplification of the definition and meaning of carbohydrates has momentous consequences. Not only does shifting to a diet low in carbs severely minimize our intake of antioxidants, complex carbohydrates, vitamins, and certain minerals, it also shifts our dietary source of energy from carbohydrates to fat and encourages consumption of protein far above the required amount.
Why is this such a terrible thing? Because the foods we choose to meet our energy needs make a big difference in whether we experience good or ill health.
Number of Calories Versus Source of Calories
If by “good and bad calories,” Taubes means “good and bad sources of energy”—in effect, good and bad foods—he and I agree, at least in principle. Plant- and animal-based foods are hugely different in terms of their nutrient contents, and watching what foods you consume is far more important than obsessing over calorie-counting without respect to where those calories come from.
Take, for example, our research into the effect of dietary protein on cancer growth in experimental animals, involving about twenty-five individual experiments conducted over about thirty years. The animals consuming the lowest amount of protein (5 percent of total calories) had far less cancer than their higher-protein-consuming counterparts, while consuming an average of 2 to 3 percent more total calories (or, as I prefer to say, more total energy). This is an important observation: more calories consumed, but less cancer.
It was not easy to convince some of my colleagues of this finding because of their long-standing and almost certain belief that our conclusion should have been exactly the opposite: that increased calories lead to increased rates of cancer (as well as other disease). These beliefs on the calorie-cancer connection were based on prior experimental studies, which showed reduced cancer occurrence when calorie consumption was reduced by a hefty 20 to 30 percent or more.14
Our finding that more calories could also mean less cancer was initially puzzling to us, too. The reason for this result, we learned through additional studies, was the effect of dietary protein on the body’s distribution and use of the consumed energy. A low-protein diet (such as a whole food, plant-based diet) increases the proportion of dietary calories expended either as body heat15 or through voluntary physical activity,16 thus sparing the storage of this energy as body fat. Our low-protein experimental animals consumed more oxygen and formed more of a highly specialized tissue (known as brown adipose tissue), which diverts calories/energy away from the making of body fat and, instead, uses it to produce body heat, a process sometimes called metabolic thermogenesis.17 In short, both processes resulting from a low-protein diet—increased thermogenesis and increased physical activity—divert calories away from the making of body fat. In these and other studies, the key difference critical to body weight loss or gain is the way that calories are used by the body, not the amount of calories consumed.
This doesn’t just happen to rats; the results of these laboratory animal studies proved consistent with our observations on humans in rural China. Calorie consumption per unit of body weight in China was significantly higher than that of Westerners,18,19 yet China’s body mass index (BMI) was substantially lower.
To use lay language, the Chinese people in the study consumed more calories but weighed less—even after compensating for their greater physical activity. Like our experimental animals, these people were eating a diet low in protein (but very high in carbohydrates!), almost all of which was provided by plant-based foods. Based on previous findings by a group of British researchers,20 it’s reasonable to assume that these people were turning the consumed calories to body heat during physical activity, just like our experimental animals. (I see this rather like the feeling of sluggishness one gets after consuming a high-fat, high-protein meal, as opposed to the energetic “light” feeling after a low-protein, low-fat meal.) Remember, too, that only a very small shift in the body’s distribution of calories (50 per day) can make an important difference in body weight even in one year.
What our findings in China suggest, then, is that consuming a whole food, plant-based, high-carbohydrate diet (in which 75 to 80 percent of total energy comes from plants) minimizes weight gain by shifting the distribution of energy to physical activity and the production of body heat rather than long-term storage as fat. Weight gain, it turns out, has little or nothing to do with the number of calories we consume and everything to do with the way those calories are used in the body.
Research (Out of) Context
These sometimes puzzling, provocative, and difficult-to-follow findings should prompt questions as to the reliability of the evidence. Taubes cites hundreds of studies to “prove” his theories. But I maintain that his conclusions—chiefly, that low-fat diets make people fat—are patently unsupported by both the historical and scientific evidence. How can I say that? The answer to this question lies in a consideration of the way research is typically done, as well as the way scientists, and Taubes and I here specifically, interpret the findings.
Taubes uses evidence from narrowly defined studies within a very complex body of evidence to create a new narrative of his own making. When isolated facts like these are knitted together, the risk that the narrative can be influenced by personal bias is higher, especially when the final product is not subjected to and/or supported by professional evaluation and scrutiny. And Taubes’ work has never been evaluated by professional, qualified peers.
In Taubes’ case, there is also something more to consider: none of the research studies he cites are his. He is not a scientist and has conducted no experimental research of his own. All of this heightens the likelihood that the narrative he has constructed from these disparate details has been impacted by his already formed prejudices. While research scientists are not immune to bias (indeed, as I describe in Whole, certain types of bias are endemic in the scientific community), the fact that they have to contend with the results of their own research, and can’t pretend to ignore them, limits to some extent their leeway to “cherry pick” facts the way Taubes has.
The way Taubes has chosen what evidence to include is a bit like the results of a prosecuting attorney having sole authority over jury selection. The jurors would likely all be honorable citizens, but they would almost certainly represent a specific slice of the total population, with characteristics and outlooks that favor the case for the prosecution.
Each of the papers Taubes references, therefore, deserves a careful examination based on a number of important issues:
♦the many experimental factors and conditions that may have impacted the paper’s results;
♦the appropriateness of the experimental study design;
♦the level of statistical significance;
♦the source of funding, not just for each particular study but for its authors in general;
♦the professional reputation of the journal; and
♦the method used for interpreting the data.
These issues are not easy to evaluate for most readers, who are not likely to be familiar with scientific research protocol. Indeed, these issues are not always easy to evaluate for experienced researchers either, especially when the researchers are not working in the immediate field of study.
I confess that I have not obtained all of Taubes’ references for my own critical review and interpretation—a task made unusually difficult by his cumbersome and questionable method of referencing.21 Thus, for expediency, I have chosen to extend to Taubes the courtesy of simply accepting, as is, the evidence (often indirect) that he believes supports the health value of the low-carb diet (lower body weight, less incidence of diabetes, etc.).
However, even if we assume the evidence to be equally valid, a problem remains: To explain the results of the studies that support the low-carb diet—the decreases in body weight, blood lipids, and, importantly, circulating insulin when initially following a low-carb diet versus the Standard American Diet (SAD)—Taubes must weave together details that, while they individually may be sound, do not accurately describe the function of the whole.
First we need to review some basics that Taubes uses in those conclusions—details about the body’s function when it comes to carbohydrates that are generally accepted as true but are in fact far from it. Though Taubes begins in the right place, his is a very narrow view of the results of energy production and metabolism as it interacts with countless other events inside the body.
When carbohydrates are consumed and the food is digested in the intestine, glucose is produced. This glucose is absorbed into the bloodstream and then, assisted by the hormone insulin, enters cells, where it is oxidized to produce energy. This satisfies our hunger—the need for energy that arises in cells and is translated to us as the desire to eat food.
Glucose not used to produce energy immediately may be stored in the liver and muscles as glycogen, a starch-like polysaccharide; it, too, is available for use by cells rather quickly, when energy is needed. There is also a second option for unused glucose: it may be converted to triglyceride (fat), a more stable storage form of energy that gradually accumulates to form adipose tissue, the stuff of obesity.22
After consuming a meal, the body’s blood glucose level rises, then returns to baseline within a few hours as the glucose is either used by cells to provide immediate energy or converted for storage. Both glucose and insulin blood levels rise and fall together in waves as we intermittently consume meals because glucose entering the bloodstream automatically triggers insulin’s release. All of this is a very normal process in healthy people.
For too many people, however, a diet high in refined carbohydrates and simple sugars results in consistently elevated glucose levels in the bloodstream. To compensate, these high glucose levels require a continuously high level of insulin that, for some as yet unknown reason, gradually loses its ability to facilitate glucose’s entry into cells. To overcome this diminished insulin activity—or “insulin resistance”—the pancreas responds by secreting still more insulin, thereby creating a vicious cycle with adverse consequences. Higher blood sugar levels lead to the release of more insulin and, if this state is prolonged, more insulin resistance, which leads to higher blood sugar levels. We might therefore consider the effects of this cycle a disease of insulin excess or, perhaps, glucose toxicity, as seen in Type 2 diabetes, obesity, and heart disease. The reason this happens, according to Taubes, is the regular overconsumption of carbohydrates.
Insulin has many other normal functions besides assisting in the cellular entry and metabolism of glucose. It also may assist in the uptake, metabolism, and storage of glucose as triglycerides (fat). Although this stored fat can be recalled and metabolized to produce energy, a high level of insulin in the bloodstream tends to block this conversion of stored fat back to energy. An overabundance of insulin therefore leaves cells elsewhere in the body hungry for energy. In response, we continue to eat—and continue to gain weight, as the body stores more glucose.
According to Taubes, the most practical solution to this problem of too much insulin in the blood is to reduce the demand for insulin by not flooding the system with high-glucose foods, especially those refined carbohydrates that are readily digested and absorbed and often produce fat.
There are a few things wrong with this, even on the surface. Although the fundamentals of this story about carbohydrate digestion, absorption, and utilization are essentially correct, it should be noted that it mostly refers to the effects of refined carbohydrates, not total carbohydrates, which are found in whole foods. In addition, the result of short-term, out-of-context findings—those obtained in the test tube, so to speak—must be reconciled with long-term health outcomes. There are many examples where a laboratory-based, out-of-context finding does not equate with a true-life experience. (Perhaps one of the better-known examples concerns the antioxidant beta-carotene, the proper form of vitamin A, which when present in food is associated with a healthy response but when consumed as a supplement causes an unhealthy response.)
I repeat: parts of what Taubes says here are definitely accurate, to the best of current scientific knowledge, and the findings he uses to construct this story may represent high-quality research. But the story itself, as well as the solution he comes to (the low-carb diet), is just not true; evidence from many other studies shows that high carbohydrate, as in the whole food, plant-based diet, also can produce fat degradation and loss of body fat. The research findings Taubes uses refer to events that have been isolated from their natural environments.
The process of combining isolated events into a cohesive story only works if the pieces of the puzzle are put into the right places. Sadly, this same process can just as easily be used to prove something that is in fact untrue. For example, if we wanted to prove that Coca-Cola promotes health, we could construct a study in which some people were given Coca-Cola to drink, while others were not given any liquid at all—and never look at the effects of Coca-Cola compared to water. This is the dilemma with almost all diet and health research: whether we have enough or the right kind of details assembled to reliably create a hypothesis that really works.
I’m not suggesting that all research looking at specific details (research that is characteristically reductionist in nature) is purposefully biased or of no value. Well-constructed reductionist studies can be used to deepen our understanding of the whole of human health by providing explanations—specific details and mechanisms—that stabilize and sustain wholistic research: research that looks not just at the evidence from one study, but at all the evidence currently available, and draws conclusions accordingly. Reductionist research must be conducted in the service of “big picture” truths that can be gleaned only from a wholistic look at reality. And this is especially true for nutrition studies.
A classic metaphor, which I explore in detail in Whole, is the old story of six blind men tasked with describing an elephant. One feels the trunk and describes the elephant as a hose. Another feels the tusk and describes a spear, a third apprehends the leg as a pillar, and so on. All of their explorations have merit, but each individual’s conclusions leads to an erroneous understanding of the thing the group has been tasked with describing. Only when the starting point is an understanding of the whole elephant can we make sense of the separate findings.
Any study that looks at only one disease, one nutrient, or one population out of context and contradicts all the wholistic evidence cannot be seen, on its own, as proof. When a reductionist finding contradicts the big picture, it doesn’t make sense to tear down that big picture. Rather, we look for exceptions, nuances, and deeper understandings—ways of reconciling an outlier data point with the demonstrated reality. Sometimes we find that the conflicting detail is a fluke (a random result of statistical uncertainty) when we repeat the experiment and fail to replicate it. Sometimes we discover that the premise of the experiment itself is flawed.
Rarely do unexplained data points bring down entire structures of thought, though it does happen on occasion; we call this phenomenon a paradigm shift. For example, Copernicus and Galileo discovered outlier data that ultimately invalidated the entire earth-centric system of astronomy that had been common knowledge since ancient times. But we can’t look at a single reductionist finding that conflicts with current theory and summarily declare the theory null and void. Outlying and contradictory data must be honored, but we honor them by following them on a rigorous search for truth, not by elevating them to dogma simply because doing so enhances our pocket-books or our egos.
This, in essence, is what the low-carb advocates are doing. By ignoring findings that comprehensively describe the whole, they elevate outlying or contradictory data to dogma.
How Low in Fat Is “Low-Fat”?
There’s one more significant way in which Taubes gets things wrong, and it has to do with a failure of definition around the term “low fat.” In fact, the misuse of their term “low fat” by the low-carb advocates is one of the most egregious misrepresentations in their entire narrative.
The low-carb-advocates’ argument in favor of a low-carb (but high-fat!) diet rests on their mistaken idea that increased dietary fat doesn’t matter—that dieters have been diligently pursuing the government’s low-fat recommendations for years, and yet no one’s getting any thinner or healthier. In fact, low-carb advocates claim, these government-recommended low-fat diets in effect cause obesity.
These pronouncements rest on the assumption that those “low-fat” dieters are actually following a low-fat diet. But this is simply not the case. It’s a myth. This so-called low-fat diet is anything but low in fat.
According to Taubes in Good Calories, Bad Calories, the inflection point tipping the nation’s scales toward a low-fat diet was the published research of University of Minnesota professor Ancel Keys in the 1950s on the connection between dietary fat and heart disease. Keys was a well-known nutritional authority prior to this work; the K-rations of World War II were formulated by and named for him. He was also known for his “starvation studies,” in which he subjected conscientious objector volunteers to near-starvation conditions to discover the effects of nutritional deprivation on human physiology.
Keys began his post-war research because of an anomalous finding: the wealthiest businessmen in Minnesota, who presumably could afford the best food and health care, were suffering a disproportionately high rate of heart disease. Keys’ intellectual pursuits had all been about starvation and the minimum calories needed by soldiers in battle conditions, so you can imagine his surprise to discover that a surfeit of rich animal foods—which were then thought to be, as they still are by most today, the highest-quality foods—appeared to make men less healthy rather than more so.
Keys’ subsequent research suggested a link between diets high in total fat, especially saturated fat and cholesterol, and heart disease. His first studies looked at Minnesota businessmen, and he later broadened his research to seven countries in four regions of the world. This Seven Countries Study23,24 published as an article in 1970 and as a book in 1980, caused quite a stir among public officials and politicians who were concerned with national health policy. In later studies, Keys broadened the scope of his research and discovered a similar effect of dietary fat on obesity, diabetes, and cancer.
According to Keys, promotion of these diseases by high-fat diets could be explained by the fact that fats, at 9 calories/gram, are calorie dense, as opposed to carbohydrate and protein, which have 4 calories/gram. High-fat diets therefore meant calorie-dense diets and more calorie consumption. This was a convenient way to combine two ideas that were popular at the time—that calories and fat each increased obesity and obesity-related diseases—into one.
Keys’ focus on fat, especially saturated fat and cholesterol, implied that consumption of foods rich in these nutrients, especially meat and eggs, should be curbed. The widespread popularity of his research also resulted in a shift in the marketplace away from the fat content of cow’s milk to low-fat and even skim milk. (On the dairy farm where I grew up, we valued milk for its butterfat content, both in the pricing of the finished milk and in the breeding programs designed to produce offspring capable of producing high-fat milk. I recall when we got word down on the farm that public opinion was moving away from high-fat milk. It was Ancel Keys’ research findings that caused the shift.)
Keys vigorously promoted his research findings, publishing two popular diet books with his wife, Margaret, (Eat Well and Stay Well [1963] and How to Eat Well and Stay Well the Mediterranean Way [1975]), alongside his scholarly work. A typical sentiment from Keys: North Americans make “the stomach the garbage disposal unit for a long list of harmful foods.”25
I had the privilege to meet Keys twice: once when he lectured at Cornell while I was a graduate student and much later when Keys, then in his nineties, was in attendance at a lecture I gave at Harvard on my research findings in China. Keys’ ultimate contribution to the field of nutrition may have been the example he set by “walking his talk”—he died in 2004, just two months shy of his 101st birthday!
Taubes claims that it was Keys, more than any other writer or researcher, who focused public attention on dietary fat as the main culprit for obesity and poor health. According to Taubes, U.S. government policy based on Keys’ research not only failed to improve our health, it also caused the very epidemics (obesity, cardiovascular disease, diabetes) that it was trying to prevent.
This interpretation is incorrect on two levels. First, Taubes assumes that Keys advocated lower consumption of saturated fat and cholesterol as the only strategy for reducing heart disease. While this is partly true, Keys was also concerned with the source of these nutrients: that is, animal-based foods. For example, he wrote while discussing the very high correlation of saturated fat with serum cholesterol in population-based studies and the “distress [it caused in] the dairy and meat industries” that these industries’ “products account for almost all of the saturated fat in Britain and the United States, and most other countries.”26 Second, to my knowledge, Keys never really defined his recommended “low-fat diet” in terms of an ideal percentage of calories from fat; he thought that relying on specific benchmarks set by policy makers did not make sense.27
In other words, while getting some of the details right, Taubes misses the nuance of this history by falsely representing the definition of a low-fat diet as well as its alleged health effects.
The very lowest level of dietary fat ever advocated by a federally funded report (one I coauthored, and the recommendations of which I was, regrettably, unable to influence as much as I would have liked) was 30 percent of daily calories.28 By no stretch of the imagination can this be considered “low fat.” A 1999 national survey showed that average dietary fat intake never dropped down to this level, at best reaching about 33 percent of total calories.29 The idea that a government recommendation to reduce dietary fat to 30 percent or lower was ever reached, or that such a level would be sufficient to demonstrate a decrease in disease, is ludicrous. It’s akin to telling smokers to cut down from five packs a day to four and a half—and then, upon seeing no results, claiming that decreased smoking doesn’t make a difference and is not worth pursuing.
Not only were the “low-fat” recommendations from this report and other sources never heeded, but the absolute intake of fat did not decrease. As a nation, we may have flirted with the idea of a low-fat diet, but we never actually succeeded in following such recommendations. While we may have reduced the percentage of our dietary fat over the last few decades (albeit slowly), because our total food intake (and calories) has gone up, dietary fat consumption, if anything, has increased.30 The suggestion that we have adhered to that 30 percent recommendation and, further, that having done so, we failed to achieve the expected health results, is fantasy. The argument by Taubes and his advocates that low-fat diets have not decreased obesity, and perhaps have even caused it, is a straw man fallacy.
To be fair to Taubes, there was a lot of focus in the scientific and health community on the evils of fat from the 1950s to the 1970s. But he and other low-carb advocates underemphasize the shift in this focus on fat, both in the health community and in public policy, that began with the 1977 McGovern Committee and the 1982 report on diet, nutrition, and cancer (the report I reference above, which proposed the lowest recommendations of calories from fat). In that report, we indicated that fat was not the main cause of cancer and other diseases, but rather a marker of the dietary proportion of (naturally low in fat) plant-based foods to (naturally high in fat) animal-based foods. In other words, a diet truly low in fat (e.g., 10 percent of calories) is by definition a diet high in good quality whole (not processed) plant-based foods and low in animal-based foods.
The McGovern report’s recommendations on dietary fat were meant to be understood in the context of the overall goal: to increase the consumption of plant-based foods while decreasing the consumption of animal-based foods. I’m confident Taubes knows this; it’s stated explicitly in the report, in the comments especially on the consumption of meat. Yet he still focuses his arguments on dietary fat and the failure of the (incorrectly labeled) low-fat diet, while ignoring the main issue: the balance of animal- and plant-based foods.
THE MCGOVERN REPORT
Let’s take a closer look at the history of the McGovern Committee report on the association of dietary fat with heart disease: both what it really said and what impact it really had. McGovern’s highly political committee was first formed in the early 1970s, after McGovern’s failed presidential bid and after his visit to the Pritikin health clinic, where he witnessed firsthand the dramatic health benefits of consuming a diet very different from the one he and most Americans followed: one truly low in fat and high in whole plant-based foods. After inviting expert testimony, the McGovern Committee recommended that dietary fat, especially saturated fat and cholesterol, be decreased, as Keys and other researchers had suggested. Because this kind of fat is far more plentiful in animal-based foods, the McGovern Committee therefore recommended reducing the consumption of meat31 as well as the consumption of “butterfat, eggs, and other cholesterol sources.” Unfortunately, the marketplace did not respond by changing the proportions of plant- and animal-based foods. Instead, politicians, marketers, and consumers alike focused specifically, and inaccurately, on the modification of their fat intake.
A preliminary 1976 recommendation by the McGovern Committee to cut back on meat consumption in general created a furor among politicians and the electorate alike. As a result, the committee revised their report in 1977 to recommend a decrease in red meat consumption but not the white meat of fish and chicken32—a political decision, not a scientific one. Even that did not prove enough of a political compromise, however. McGovern personally told me that several prominent Midwest senators subsequently lost their 1980 elections because their support for his committee’s recommendations upset their political base of livestock farmers. Professor Mark Hegsted, who was on leave from Harvard University and acting as a full-time expert consultant to the McGovern Committee staff, told me several stories about exceptionally hostile reactions from certain groups to these plant-focused recommendations. Even though the McGovern report only concerned the effect of diet on cardiovascular disease, the public furor—or that of the lobbyists, anyway—was intense. I remember wondering at the time what kind of adverse reaction might occur were there to be a similar focus on dietary effects on cancer, the much more feared disease.
Shortly thereafter, a U.S. Senate Committee wondered the same thing. They organized a public hearing and asked the director of the National Cancer Institute (NCI), Vince DeVita, for testimony. During that testimony, DeVita said that he could not be sure if the McGovern Committee’s recommendations about the effects of diet on heart disease would similarly apply to the effects of diet on cancer.33 Hearing this, the Senate Committee appropriated about $1 million for the NCI to organize an expert committee at the NAS to review the existing literature on the topic. I was invited, along with twelve others, to be on this committee, which eventually produced the landmark 1982 NAS report on diet, nutrition, and cancer.34 Although we recommended reducing dietary fat to 30 percent or less of total dietary calories—a level similar to that in the McGovern report on heart disease—we also suggested, as a goal (versus the more proactive “recommendation”), the increased consumption of whole foods such as fruits, vegetables, and grains.
As expected, the release of this report fanned the flames of public discussion about food and health. According to the NAS, it was the most sought-after report in their history. I appeared on the PBS show McNeil-Lehrer News Hour and was featured in People, among many other magazines, to discuss the report. And, as with the McGovern Committee report, political fallout was intense. A prominent task force of the agricultural industry, the Council for Agricultural Science and Technology (CAST),35 quickly responded; within two weeks, they had published a very critical commentary of our report and placed copies of it on the desk of every congressperson and senator. A few of us testified to congressional committees about it.
Our goal (not a recommendation) in the NAS report36 to reduce dietary fat to 30 percent or less was not merely an attempt to mimic the McGovern Committee’s similar recommendation. It was intended to emphasize the dietary change that we thought worth pursuing for cancer control, based on the available evidence at that time. We stated in our executive summary that the evidence on cancer suggested an ideal diet considerably lower in total fat than our 30 percent goal—perhaps 20 percent of calories or lower—which would put even more emphasis on naturally low-fat whole plant-based foods. We chose the arbitrary and more conservative benchmark of 30 percent because going lower might have suggested a decrease in consumption of protein, especially animal-based protein, and politicians then, as now, were sensitive to the interests of dairy and livestock organizations.
The 30 percent dietary fat goal was not intended to single out fat or any other nutrient as the specific and only dietary effector of cancer. The report heavily emphasized the consumption of whole foods, especially fruits, vegetables, and grains. In doing so, we clearly stated that none of our specific goals applied to individual nutrients, such as adding individual micronutrients in supplement form or subtracting fat.
As marketplace events developed, however, considerable emphasis was given to individual nutrients such as fat (eat less), fiber (eat more), and vitamins and minerals (take supplements). These and other similar responses have been the source of one of my greatest frustrations regarding the way science is interpreted and communicated to the general public. It seems that whenever whole plant-based foods are brought up for discussion, the conversation turns in some way to the exploitation of single nutrients, whether they are fat, carbohydrates, protein, or vitamin and mineral supplements. That’s where the money was and still is.
Still, recommendations during the 1980s and 1990s by respected institutions to increase consumption of plant-based foods continued to be published,37,38 leading up to the 1997 World Cancer Research Fund/American Institute for Cancer Research report,39 which I co-chaired. The first recommendation of this 1997 report bluntly stated: “Consume a plant-based diet.”
In Good Calories, Bad Calories, Taubes grossly oversimplifies and distorts the history of the diet and health field. He makes it seem as if the entire field is focused only on dietary fat as an evil nutrient and, further, that scientists found a dietary level of 30 percent fat to be sufficiently “low.” Rather, the most important message surfacing during the period from the 1970s to the 1990s was to increase consumption of whole plant-based foods and, by inference, to decrease consumption of animal-based foods.
Taubes, unfortunately, is not the only one who missed that message; most of the public did, too.
THE OPTIMAL HUMAN DIET FOR IDEAL WEIGHT, VIBRANT HEALTH, AND LONGEVITY
Good science tells us the optimal way to eat is what I call the Whole Food, Plant-Based (WFPB) diet. This is something the evidence had been clear on long before I was considering my lab’s own experimental findings. Many decades earlier, everyone was regularly advised, if vaguely, to “eat more fruits and vegetables.” But this may be the first time you’ve encountered this much evidence for the remarkable health-promoting effects of a WFPB diet. Not because the idea is “fringe” or the evidence is weak; rather, because the food, medical, and pharmaceutical industries have a lot to lose if our society wises up to the health-giving properties of whole, plant-based foods and the disease-causing properties of animal-based and highly processed foods. The evidence points clearly to a WFPB diet as the one that can most reliably deliver radiant long-term health, as well as the slim bodies we desire.
First, a definition. The WFPB diet consists of whole foods—that is, foods as close to their natural state as possible. A wide variety of fruits, vegetables, grains, nuts, and seeds make up the bulk of the diet. It includes no refined products, such as white sugar or white flour; no additives, preservatives, or other chemical concoctions, which our bodies were never programmed to recognize or digest; no refined fats, including olive or coconut oils; and minimal—or, better yet, no—consumption of animal products, perhaps 0 to 5 percent of total calories at most.
By consuming a broad range of plant foods, we don’t really have to worry about the specifics of calories, carbohydrates, fats, protein, or even vitamins; the numbers more or less take care of themselves. Since plant foods are largely carbohydrate based, the percentages of calories tend to approach 80 percent from carbohydrates, 10 percent from protein, and 10 percent from fat. Of course, if you continually binge on avocados and nuts and avoid leafy greens, you can distort the spirit of the diet. But even with your best efforts, you’d be hard-pressed to reach even as much as 15 percent of your total calories from protein with a WFPB diet.
Could you just increase your consumption of total protein-from animal sources and still get the desired benefits of a WFPB diet? Yes, but getting 15 percent of your calories from plant protein is not the same as getting 15 percent of your calories from animal protein, at least in part because of the major difference such a change would make in the consumption of other nutrients that accompany animal-based foods.
In my first book, The China Study: The Most Comprehensive Study of Nutrition Ever Conducted and the Startling Implications for Diet, Weight Loss, and Long-Term Health (2004), which I coauthored with my son Tom, I shared the research that my lab and many other scientists had accumulated to demonstrate the remarkable health effects of the WFPB diet. In my second book, Whole, I discuss why this evidence is more reliable and accurate than the science that supposedly supports high-animal-foods diets. For the full story, I recommend those books. For our purposes here, I’ll give you the short version.
As summarized in The China Study, the WFPB diet provides an exceptionally rich bonanza of antioxidants, complex carbohydrates, and optimum intakes of fat, protein, vitamins, and minerals, many of which contribute to disease prevention. Any deviation from this model—as with consuming animal-based or processed foods—causes you to miss out on the vast benefits of these life-sustaining nutrients. For the most part, supplementation and fortification with individual nutrients or combinations thereof will not restore what whole foods can do for health.
Moreover, and very much to the point for this book, the “high-carb” WFPB diet decreases the risk of obesity-related degenerative diseases—in direct opposition to what Taubes’ model of sharply reduced carbohydrate consumption predicts.
Effects on Glucose: The WFPB Diet Versus the Low-Carb Diet
As you’ll recall, Taubes’ model states that a low-carb, high-animal-protein diet will reduce blood glucose, insulin, and cholesterol, thus decreasing the risk for obesity, diabetes, and heart disease. But many reports show, in various ways, that the opposite is true.
My friend David Kritchevsky, who was probably the leading researcher in this area until his death, found40 that “protein of animal origin is more cholesterolemic [leading to higher cholesterol in the bloodstream] and atherogenic [contributing to heart disease] than protein of plant origin for rabbits,” citing several studies41—a distinction between types of protein that was first noted in regard to atherosclerosis more than sixty years ago.42 He found the same to be true for humans, as well.43 We observed a similar distinction between soy and casein protein (the principle protein in milk) in my lab when they were compared in our studies on experimental cancer with rats.44
Likewise, animal and plant protein have completely different effects on insulin. Dr. Richard Hubbard of the Loma Linda School of Medicine and his colleague Albert Sanchez have done significant research on the effects of plant- and animal-based proteins,45 on findings that directly concern Taubes’ model. According to their research, plant protein actually decreases insulin and increases glucagon (the counterweight to insulin), preventing or reversing diabetes. A higher plant protein/animal protein ratio represses the formation of fat (triglycerides), while reducing the activity of a key enzyme in the synthesis of cholesterol. In short, the persistently low insulin levels commonly observed with plant protein–based diets (as with the WFPB diet—though not, importantly, with diets high in refined carbohydrates) are associated with persistently low blood cholesterol levels, among other biomarkers of diseases like heart disease, obesity, many cancers, and other serious ailments that track together in populations.
What this means is that the high-carb, plant protein–based WFPB diet behaves exactly the opposite of how Taubes predicts it will. Taubes says that a high-carb diet increases insulin, which converts the high blood sugar to fat and then represses the conversion of the fat back to energy, leaving fat stored in the cells—and this is why people get fat and eventually suffer from diabetes and other diseases associated with obesity. Although this may sound attractive and may be true for people consuming a diet high in refined carbohydrates (i.e., sugar), there is no evidence that this applies to a WFPB46,47,48 diet that is high in total carbohydrate and low in protein, all of which is plant based. Virtually every person who uses the WFPB diet loses weight, reduces their blood sugar and insulin levels, and resolves diabetes and related diseases. A plant protein–based diet (as in the high-carb WFPB diet) also decreases total blood cholesterol and the formation of plaques that lead to heart disease, effects not seen from a low-carb, animal protein–based diet. In direct refutation of Taubes’ predictions, the WFPB diet also successfully promotes weight loss, and it does so without the serious side effects that accompany the low-carb diet.
I summarized the side effects of the low-carb diet earlier: more headaches, bad breath, constipation, and muscle cramps. The low-carb diet shows little or no consistent health benefits when compared with other diet strategies, which are free of these side effects. And if apparent benefits do occur on the low-carb diet—weight loss, in particular—they are not sustained. In addition to being both inconsistent and relatively small, the alleged health benefits tend to disappear within a year.49 But more to the point, the low-carb diet’s ability to show any benefit depends on the control diet against which it is compared.
Low-Carb Diet “Benefits” in Context
Usually the low-carb diet is evaluated by comparing it to the Standard American Diet (SAD)—which, as we’ve seen, is misleadingly labeled “low fat” when in reality (and compared to the WFPB diet, in which only 10 percent of the calories come from fat) it’s high in fat, as well as high in animal protein and low in antioxidants and complex carbohydrates. About 30 to 40 percent of the SAD’s calories come from fat. This is a huge difference! The SAD is also, on average, about 70 percent higher in total protein than the amount recommended and easily provided by a WFPB diet (meaning that the protein consumption of about half of Americans is even higher than that). Almost all of this excess protein is from animal-based foods. To put it another way: at least 90 to 95 percent of Americans are consuming a carbohydrate-poor, relatively rich diet that is already near Atkins levels in its inclusion of animal protein.
Because of this similarity, when an Atkins/Taubes low-carb diet is compared with modest variations of the SAD, any observed beneficial effects are mostly random and relatively trivial, though that doesn’t prevent the low-carb spin masters from making them into headlines whenever possible. A true dietary comparison, by contrast, would also include the WFPB diet—but this almost never happens.
Nowhere is this more clear than in a 2007 study by Gardner et al.50 The study’s objective was to compare the ability of four popular diets to reduce body weight, and their particular focus was on investigating if low-fat diets were actually able to reduce body weight. Therefore, the flaw that I found especially repugnant—and obvious—was their failure to use a truly “low-fat” diet for comparison: they compared the results of Atkins and several other diets to what they claimed was the Ornish diet (a low fat, whole plant food diet based on the work of Dr. Dean Ornish, a pioneer in the use of a WFPB diet to reverse heart disease).
The true Ornish Diet, like the WFPB diet, contains only 10 to 12 percent fat. But the authors of this Atkins-friendly research paper instead used a grossly distorted version of the Ornish Diet, one that contained 29 percent fat, and called it “extremely low fat”! The distortion was even more serious because the authors’ so-called Ornish Diet also contained 18 percent protein, which is 70 to 80 percent higher than the amount generally present in plant-based diets. In the Gardner et al fabricated Ornish Diet, fat and protein comprised 48 percent of total calories, rather than the 20 to 22 percent in the true Ornish plan.
The other diets used for comparison were two very similar variations on the SAD: the LEARN51 and Zone52 diets. Together, these four nutritionally similar diets were severely limited in their ability to show meaningful and statistically significant differences, due to their similarities in dietary fat and protein (the two measures that best represent the differences between these plans and a truly low-fat, low-protein, WFPB diet): fat and protein accounted for 65, 54, 51, and 48 percent of total calories, respectively, which are all far in excess of the WFPB diet’s 22 percent. Of course, there was one scientifically random difference observed at the end of the study: they found a slightly lower body weight for the Atkins Diet than the SAD and Ornish Diets, and this scientifically nonsignificant finding made headlines as if it were extremely important.
Because this study was destined to create major media attention, it required critique at the time it was published in the acclaimed Journal of the Medical Association (JAMA). Critique in conventional science generally occurs in the widely accepted letters-to-the-editor format, which might be considered another aspect of the peer-review process. Four of us in the profession therefore duly submitted our letters to the journal editor to point out the study’s serious flaws and seek the investigators’ responses. Usually such letters are published after some modest peer review—but not in this case. The JAMA editor denied all four of our critique letters, including one letter from Dr. Ornish himself, the man whose diet was being so grossly misrepresented. Over the course of my career, I have published many research papers and served on several science journal editorial review boards, and never have I witnessed such unprincipled and unsavory behavior. Readers had a right to hear both our critiques and the researchers’ responses to them, but instead they heard nothing. And so this study, like many similar findings, went unchallenged and has since been asserted as foundational evidence proving the superiority of the low-carb diet.
Another recent and highly publicized study also failed to include diets of sufficient nutrient difference that would have enabled the researchers to analyze and discern their effects and thus evaluate and understand the different diets in their proper context. The study, “Primary Prevention of Cardiovascular Disease with a Mediterranean Diet,”53 published in the New England Journal of Medicine, concerned the supposed health benefits of the Mediterranean diet in regards to heart attack and stroke. Its participants, who were all at high cardiovascular risk but did not have cardiovascular disease at the time of the study, were randomly assigned to one of three diets: “a Mediterranean diet supplemented with extra-virgin olive oil, a Mediterranean diet supplemented with mixed nuts, or a control diet (advice to reduce dietary fat).”
According to the researchers, their findings showed that both versions of the Mediterranean diet—the one with added olive oil and the one with added nuts—were healthier than a standard low-fat American diet. The “low fat” group suffered 109 “events” (strokes and heart attacks), compared to just 96 for the Mediterranean olive oil group and 83 for the Mediterranean nuts group.
At first glance, you might agree with the researchers (and the low-carb hucksters) who called this finding a major blow in the battle against misguided low-fat dieting. But diving a little deeper into this research reveals something very different.
Before I tell you the actual numbers reported by the researchers, take a wild guess at the percentages of fat in the three diets. You’d think that a diet described as “low fat” would include a lot less fat than those touted as “low carb,” right? Well, you’d be wrong.54 By the end of the trial, the two Mediterranean diet groups were getting a little more than 41 percent of their calories from fat, while the so-called “low fat” control group was getting 37 percent of their calories from fat.
Thirty-seven percent of total calories from dietary fat is considered a low-fat diet? Four percent is a significant difference in dietary fat consumption?
Just for fun, let’s graph these results and compare them to SAD and WFPB diets:
Here’s what the headlines should have read: “Three almost identically bad diets produce almost identically bad health outcomes.”
I cannot overstate the seriousness of this distortion of what constitutes a low-fat diet, or how common this distortion appears in scientific papers published by low-carb advocates. There have been three relatively recent reviews of the low-carb diet as compared with other diets, published in 2003,55 2006,56 and 2009,57 respectively. These summaries are quite repetitive, mostly including the same research studies, in which the subjects are generally overweight to obese. Each report concludes that, on average, low-carb-diet interventions generally result in some weight loss and favorable but variable changes in indicators of cardiovascular disease risk (conclusions that are highlighted in the abstracts, which provide the main and only information from these studies that most laypeople will see). And throughout this literature, we see the same misinterpretation of a “low-fat” diet and the same lack of diversity across diets repeated ad nauseum. “Low fat” is always approximately 30 percent fat (or higher), not the WFPB diet’s 10 to 12 percent fat. In these studies, both the control diet and the low-carb diet are high in animal protein and low in plant-based foods, making it very difficult to see the results we know exist when a much wider range of nutritional compositions are available for comparison.
THE WHOLE TRUTH ABOUT LOW-CARB
Low-carb advocates have succeeded in winning over a substantial segment of the market for about four decades now. In part, they have done so because their message is one that many people want to hear: good things about their bad habits.
Over the years, I have found it increasingly difficult to accept low-carb advocates’ antics. They’ve changed the benchmark for the definition of a “low-fat” diet and seemed normal. The consumption of high amounts of animal protein. They’ve used the concept of “low-carb” to negatively reflect on the source of carbs: whole, plant-based foods. And they’ve done these things for their own self-serving interests: protecting and even expanding the marketing horizon for high-fat, animal protein–based foods. Taubes and many other low-carb advocates use an abundance of carefully selected but out-of-context details to add a scientific patina to their arguments, which just don’t hold up under careful scrutiny. Please don’t get me wrong: such details can be, and are, useful when they are employed to describe an accurate whole. But when details are spun into a false narrative to support a diet with unpleasant side effects and serious long-term consequences, it’s time to sound the alarm, loud and clear.
When describing their diet, either in research or in general discussion, low-carb advocates usually compare it to our already poor Standard American Diet (SAD) and/or the only slightly modified “low-fat” version recommended by the government. As we’ve seen, this is a false comparison. Our diet or even its slightly modified government-sanctioned version is not what the low-carb people claim it is. First, the SAD is already high in total protein—about 70 percent higher than ideal—and around 70 percent of it is protein from animal-based foods (thus limiting consumption of plant-based foods and their antioxidants and complex carbohydrates). Second, the SAD contains three to four times the amount of fat the science recommends. In short, it is a fat-rich, protein-rich, and often refined carbohydrate–rich diet. This is the benchmark that’s called “low fat” by the low-carb advocates, and this is what they use to prove their diet’s superiority over all other types of eating. These are very serious misrepresentations.
To say that the government-recommended “low-fat” diet adopted during the past four decades has only led to more obesity is hubris squared. Even if the American public had followed the recommendations and reduced their dietary fat (and the most one could say, in that case, was that dietary fat was reduced from about 35 to 33 percent of total calories), that cannot be used to properly evaluate the health benefits of a truly low-fat diet like the WFPB diet, in which only 10 to 12 percent of calories come from fat.
I am confident that low-carb advocates like Taubes know all this. But rather than allow this to expose their argument for the embarrassment it is, they try to explain these facts away by pejoratively describing the WFPB diet (as with the Ornish Diet in Gardner et al.58) as “extreme.” Actual low-fat diets are almost never taken into account in these discussions, and when they are, they are distorted to make them more similar to the SAD. In so doing, low-carb advocates cleverly remove the possibility of experimentally observing the real, life-and-death differences between these diets.
Low-carb advocates also focus on weight—not on health. The low-carb diet cannot reverse and sustain the reversal of advanced diseases like the WFPB diet can. When the dietary practices in different countries are compared, high-fat, high-protein diets (like the low-carb diet) are consistently associated with higher, not lower, rates of several cancers, heart disease, and other diseases. Plant-based diets show the opposite effect. In fact, I do not know of a single study among the hundreds undertaken where it has been shown that a low-carb (high-protein, high-fat, low-fiber/complex carbohydrate) diet is associated with less cancer, heart disease, or diabetes.
Perhaps the most telling report on the low-carb diet and health is the recent summary of 17 studies published in January 2013 involving 272,216 subjects,59 in which a low-carb diet showed a statistically significant 31 percent increase in total deaths. This finding is even more telling than the statistics suggest because this 31 percent increase is in comparison to the already high mortality typically observed for the SAD, when compared to a whole food, plant-based diet. Also, this study is the first opportunity for us to consider low-carb claims and inferences based on long-term population-based data from multiple nations. These findings, and the inability of the low-carb diet to reverse serious diseases like heart disease and Type 2 diabetes, makes the initial decreases in body weight often observed with the low-carb diet “irrelevant,” as the authors of this report note.
Low-carb advocates like to discount such population-based studies because they do not allow us to determine causality. But this complaint is valid only when made against investigations that have been designed to look for specific, single-nutrient or single-chemical causes of disease. This is not how nutrition works. The dismissal is much less valid when an investigation is looking for associations between broad classes of food—as is the case in these studies, which looked for effects on a broad class of disease outcomes from broad classes of foods that owe their effects to broad classes of nutrients.
The only health claim low-carb advocates make that is worthy of positive note is their warning against refined carbohydrates (refined flours and sugars). But even then, they use this warning largely to try to make a larger point: that all “carbs” are bad. They invented the word “carb” and use it to paint all carbohydrates—all plant-based foods, since these are the sole source of carbohydrates—with the same brush. It’s long been documented that refined carbohydrates—carbohydrates that are no longer in their natural, wholistic form—cause health problems. That does not mean that we can use this finding to smear complex carbohydrates, including fiber and starch, in general.
The arguments for the low-carb diet are built entirely from out-of-context, highly reductionist results, woven together into a picture that does not reflect either the summation of scientific data or the reality of health. And that health—not just short-term, unsustainable weight loss, but true, lasting, vibrant health—whether it be for individual people, for entire societies, or for the planet, is the goal to which we all should aspire.
It is time that the low-carb diet, and its alleged benefits, be dismissed as a serious fraud. It is only a continuation of the already poor nutritional status offered by the standard American diet, in a direction that actually makes our individual and collective health worse.
APPENDIX:THE PALEO DIET
In the preceding text, I listed several variations on the low-carb diet, including Mary Dan and Michael Eades’ Protein Power, Barry Sears’ Enter the Zone, Peter D’Adamo’s Eat Right 4 Your Type, Arthur Agatson’s South Beach Diet, and Eric Westman’s The New Atkins for a New You. But the version that has been getting the most attention in recent years is The Paleo Diet. First published in 2002 and written by Loren Cordain, an exercise physiology professor at Colorado State University, its basic message emphasizing high protein consumption is now offered in dozens of versions and formats, according to Amazon listings. That message, at its core, is low carb. It’s especially so by whole food, plant-based diet standards: it allows for, and even encourages, a diet that includes as much as 30 to 50 percent of calories from fat and 30 to 50 percent from protein, leaving only a small amount of calories to be supplied by carbohydrates. (Compare that to the WFPB diet’s 8 to 12 percent from fat and 8 to 12 percent from protein.) This “Paleo” book and its imitators may soon become the most popular contenders in the low-carb genre, if they aren’t already. So what’s my take?
There are a number of low-carb gurus offering advice on how to eat, but, to my knowledge, Cordain is one of only two who have published in the peer-reviewed experimental research literature (the other being Eric Westman at Duke University), a practice that I strongly respect. So let’s begin there, with Cordain’s research.
Cordain bases his views on the highly conjectural dietary habits of the Paleo (Stone Age) people, as well as their contemporary counterparts, modern-day hunter-gatherers whose diets, he suggests, can be studied as surrogates for those eaten during Paleo times. However, he confesses in several places in his research papers60 that estimates of dietary intakes in both of these groups are “subjective in nature.” He also acknowledges that “scores” attempting to rate these presumed intakes from a very large compendium of 862 of the world’s societies61 “are not precise.” Further, he notes that the true “hunter-gatherer way of life”—one not influenced by Western life—“is now probably extinct.” Thus researchers “must rely on indirect procedures to reconstruct the traditional diet of pre-agricultural humans.” This is an honest but rather apologetic view of this research.
Prior to 2000, anthropologists seemed to have reached a consensus, arising from a 1968 publication by Richard Lee,62 that across fifty-eight different hunter-gatherer societies, only about 33 percent of the consumed foods were animal-based. In a research paper63 in 2000, however, Cordain introduced a very different estimate. Unlike Lee, Cordain included fish in his definition of animal-based foods, and he added a larger number of hunter-gatherer societies for his review (229 as opposed to fifty-eight). Cordain then concluded that 66 to 75 percent of these “Paleo” diets represented animal-based foods—a proportion at least twice as high as Lee’s earlier estimate.
By broadening the scope of his research in this way, Cordain substantially shifted the conversation. Now, instead of ancient dietary habits being regarded as primarily plant-based, they are considered to be animal-based. Cordain claims that his new estimate is supported by another, “more exacting” report64 conducted on a smaller sample of hunter-gatherer societies, which concluded that 65 percent of these diets were animal-based—very close to Cordain’s own estimate of 68 percent.
In his work, Cordain enthuses about humans being rather carnivorous, suggesting that “hominids may have experienced a number of genetic adaptations to animal-based diets early on in our genus’s evolution analogous to those of obligate carnivores such as the feline.”65 He goes on to say that “even when plant food sources would have been available year round at lower [tropical] latitudes, animal foods would have been the preferred energy source of the majority of worldwide hunter-gatherers” and, further, that “the tissues of wild animals would have almost always represented the staple food for the world’s contemporary hunter-gatherers.” Like other low-carb proponents, Cordain regards the consumption of animal-based foods as an almost sacred part of the human tradition, with deep roots in our distant past.
Cordain’s new interpretation of early human diets has been challenged, on several grounds, by the scientific literature. First, according to anthropologist Katherine Milton,66 Cordain’s assumption that contemporary hunter-gatherers are representative of historical hunter-gatherers could be a stretch. Most of the earlier hunter-gatherers had vanished or been pushed into marginal environments before present-day surveys on hunter-gatherers were collected (a view shared by Cordain67). Accordingly, it is questionable if these more recent hunter-gatherers are the “survivors [representing] the primitive condition of mankind.”68
Second, Cordain’s provocative idea that humans “may have experienced a number of genetic adaptations to animal-based diets” like carnivorous felines is really only a conjecture (note his use of “may have”). To my knowledge, there is no evidence that genetic adaptations favoring the consumption of animal-based foods could have occurred on the scale required to convert early humans into true carnivores.69
Third, humans cannot synthesize their own vitamin C, which is made only in plants. Other mammals that require vitamin C are all plant eaters; mammals whose diets are primarily carnivorous, in contrast, don’t require it. Why would humans be any different?
Fourth, for most of their early history, humans did not have the speed or strength to catch and slaughter larger animals for food, making the possibility of diets high in animal protein rather low. (However, Cordain does make a reasonably plausible argument for the possibility that some prehistoric groups did regularly hunt animals, mostly dependent on the high energy return hunters would have received in exchange for the energy expended in hunting70).
Fifth, human anatomy compares well with that of our nearest living nonhuman primate relatives, like chimpanzees, who do and always have mostly relied on plants for dinner. We share a similar gut anatomy (simple acid stomach, a small intestine, a small cecum, and a markedly sacculated colon), and the diets of these near-relative nonhuman primates contain only 4 to 6 percent animal-based food, most of which consists of termites and ants.71 (Cordain, in fact, presented a very similar estimate for the amount of meat in prehistoric humans’ diets—3 to 5 percent—in a 2004 symposium in Denver, Colorado [a symposium that hosted a talk by me as well].)
These points taken together form a more than adequate argument against the reliability of Cordain’s rather sweeping claims about the animal-food-oriented nature of prehistoric humans’ diet. I cannot understand how the Paleo Diet enthusiasts are so certain of their views based on evidence that is so conjectural and uncertain—and so at odds with modern-day findings, obtained using research methodologies that are far more direct and robust. Using crude approximations of what ancient people may have eaten as primary evidence for what we should be eating today makes very little sense to me. Using evidence obtained from contemporary hunter-gatherer people as a surrogate raises the same uncertainty, especially when these contemporary groups’ diets are likely to have been greatly altered from those of earlier times.
Also add to these concerns the highly questionable nature of animal-versus-plant-food dietary estimates taken from archaeological studies, given that plant foods leave little or no trace in fossilized remains. Further, what do we know about the lifespans of prehistoric people? Did they live long enough to suffer the diet-dependent degenerative diseases of aging? Evolutionary arguments that draw conclusions about health impacts beyond the ages of fertility, after one is no longer able to pass on one’s genes, are not especially convincing, and if our ancestors did not live long enough to develop these diseases, then fossil remains cannot be used as evidence to draw conclusions about their long-term health.
I agree that humans must have consumed some amount of animal-based food during their evolutionary past. But I don’t agree that we should use highly questionable evidence from ancient history to vigorously assert the correct amounts of protein and fat to be consumed in the present day, when we have access to far superior research methodologies and experimentation.
Like other low-carb advocates, Cordain fails to explain or even mention evidence that sharply contrasts with his hypothesis, especially evidence that supports the health value of the wholefood, plant-based diet. For example, it has long been established that when diet and disease correlations for different populations are compared (as in cross-sectional studies), diets rich in fat and animal protein (like the Paleo Diet) correlate strongly with higher rates of heart disease and cancers of the breast, colon, and prostate,72 to name only a few. (Although I mention cross-sectional correlation studies, I am not inferring specific causality from these correlations; I am only saying that this long-established and indisputable relationship—the high ratio of animal to plant foods, expressed in various ways—categorically refutes the main tenet of the Paleo/low-carb advocates.) I know of no studies, for example, showing that a Paleo/low-carb diet is associated with lower rates of these and other related Western diseases. There is absolutely no wiggle room here.
Another profound effect that Cordain and other low-carb advocates ignore concerns the substantial health benefits that are quickly observed when people adopt a WFPB diet. When switching to the WFPB diet from the current American diet that is only marginally less high in fat and protein than the Paleo/low-carb diet, the health benefits are broad, surprisingly rapid, and relatively free of side effects. I know of no evidence yet produced showing that the Paleo/low-carb diet can do this, marking a truly striking difference between the Paleo/low-carb diet and the WFPB diet.
In general, when following the WFPB diet, serious illnesses like heart disease,73 diabetes,74 and certain cancers (including cancer of the liver75 and pancreas76 and melanoma77) and autoimmune diseases are not only prevented but, more important, can be intercepted in their forward progress and even reversed (as reviewed in The China Study). The evidence on treating these diseases has been published in peer-reviewed professional journals, and I am confident that, in the near future, these same benefits will be shown for a broad spectrum of additional disease conditions.
You can read much more in The China Study (as well as in popular books by physicians Dean Ornish,78 Caldwell Esselstyn,79 John McDougall,80 Neal Barnard,81 Joel Fuhrman,82 Pamela Popper,83 among many others), but the evidence is remarkably consistent: when eating the WFPB diet—a diet that is exactly the opposite of the Paleo Diet—the benefits begin quickly, slowing and often reversing a broad spectrum of diseases and illnesses. Has a Paleo/low-carb diet ever been shown to do this? No. Not ever. And while more formal, peer-reviewed research still needs to be done on the comprehensive effects of the WFPB diet, the experimental, observational, and clinical evidence provides a remarkable degree of consistency. This type of evidence profoundly trumps any theoretically mechanistic or “archeological” evidence the Paleo Diet has to offer.
PREVIEW OF WHOLE: RETHINKING THE SCIENCE OF NUTRITION
T. Colin Campbell, PhD,with Howard Jacobson, PhD
INTRODUCTION
In 1965, my academic career looked promising. After four years as a research associate at MIT, I was settling into my new office at Virginia Tech’s Department of Biochemistry and Nutrition. Finally, I was a real professor! My research agenda couldn’t have been more noble: end childhood malnutrition in poor countries by figuring out how to get more high-quality protein into their diets. My arena was the Philippines, thanks to a generous grant from the U.S. State Department’s Agency for International Development.
The first challenge was to find a locally produced, inexpensive protein source. (Even though malnutrition is largely an issue of not getting enough calories overall, in the mid-1960s we thought that calories from protein were somehow special.) The second challenge was to develop a series of self-help centers around the country where we could show mothers how to raise their children out of malnutrition by using that protein source. My team and I chose peanuts, which are rich in protein and can grow under lots of different conditions.
At the same time, I was working on another project at the request of my department chair, Dean Charlie Engel. Charlie had secured U.S. Department of Agriculture funding to study aflatoxin, a cancer-causing chemical produced by a fungus, Aspergillus flavus, and my job was to learn all I could about how the fungus grew so we could prevent it from growing on various food sources. This was clearly an important project, as there was quite a bit of evidence that Aspergillus flavus caused liver cancer in lab rats (the mainstream assumption was, and still is to this day, that anything that causes cancer in rats or mice probably also causes cancer in humans).
I soon discovered that one of the main foods Aspergillus flavus contaminates is … peanuts. In one of those cosmic coincidences that appears amazing only years later, I found myself studying peanuts in two completely different contexts simultaneously. And what I found when I looked deeply into these two seemingly unrelated issues (protein deficiency among the poor children of the Philippines and the conditions under which Aspergillus flavus grows) started to shake my world and caused me to question many of the bedrock assumptions on which I and most other nutritional scientists had built our careers.
Here’s the main finding that turned my worldview—and ultimately, my world—upside down: the children in the Philippines who ate the highest-protein diets were the ones most likely to get liver cancer—even though the children with high-protein diets were significantly wealthier and had better access to all the things we typically associate with childhood health, like medical care and clean water.
I chose to follow this discovery everywhere it led me. As a result, the trajectory of my career veered in unexpected and unsettling directions, many of which are detailed in my first book, The China Study. I ultimately became aware of two things: First, nutrition is the master key to human health. Second, what most of us think of as proper nutrition isn’t.
If you want to live free of cancer, heart disease, and diabetes for your entire life, that power is in your hands (and your knife and fork). But sadly, medical schools, hospitals, and government health agencies continue to treat nutrition as if it plays only a minor role in health. And no wonder: the standard Western diet, along with its trendy “low-fat” and “low-carb” cousins, is actually the cause, not the cure, of most of what ails us. In a nutshell, the “miracle cure” science has been chasing for the past half century turns out not to be a new wonder drug painstakingly formulated after decades of brilliant and relentless lab work or a cutting-edge surgical tool or technique using lasers and nanotechnology or some transformation of our DNA that will turn us all into immortal Apollos and Venuses. Instead, the secret of health has been in front of us all along, in the guise of a simple and perhaps boring word: nutrition. When it comes to our health, it turns out the trump card is the food we put in our mouths each day. In the process of learning all this, I also learned something else very important: why most people didn’t know this already.
The medical and scientific research establishments, far from embracing these findings, have systematically dismissed and even suppressed them.
Few medical professionals are aware that our food choices can be far more effective shields against disease than the pills they prescribe.
Few health journalists report the unambiguous good news about radiant health and disease prevention through diet.
Few scientists are trained to look at the “big picture” and instead specialize in scrutinizing single drops of data instead of comprehending meaningful rivers of wisdom.
And paying the piper and calling the tune for all of them are the pharmaceutical and food industries, which are trying to convince us that salvation can be found in a pill or an enriched snack food made from plant fragments and artificial ingredients.
The truth. How it’s been kept from you. And why. That’s what this book is all about.
WHY ANOTHER BOOK?
If you’ve read The China Study, you’ve heard some of this before. You know the truth about nutrition, and you’ve heard a little bit about the resistance I and other scientists have faced in trying to bring this truth to light.
Since its publication in 2005, millions of people have read or read about The China Study and shared its insights with friends, neighbors, colleagues, and loved ones. Not a day goes by that I don’t hear grateful testimonials to the healing power of whole, plant-based foods. Anecdotal as each of these stories may be, the overall weight of their combined evidence is substantial. And each of them is more than ample compensation for the troubles and obstacles placed in my way by powerful interests who make money from our collective ignorance.
Also, since 2005, many of my colleagues have conducted varied studies that show even more powerfully the effects of good eating on the various systems of the human body. At this point, any scientist, doctor, journalist, or policy maker who denies or minimizes the importance of a whole food, plant-based diet for individual and societal well-being simply isn’t looking clearly at the facts. There’s just too much good evidence to ignore anymore.
And yet, in some ways, very little has changed. Most people still don’t know that the key to health and longevity is in their hands. Whether maliciously or, as is more often the case, due to ignorance, the mainstream of Western culture is hell-bent on ignoring, disbelieving, and, in some cases, actively twisting the truth about what we should be eating—so much so that it can be hard for us to believe that we’ve been lied to all these years. It’s often easier to simply accept what we’ve been told, rather than consider the possibility of a conspiracy of control, silence, and misinformation. And the only way to combat this perception is to show you how and why it happened.
That’s why this new book felt necessary. The China Study focused on the evidence that tells us the whole food, plant-based diet is the healthiest human diet. Whole focuses on why it’s been so hard to bring that evidence to light—and on what still needs to happen for real change to take place.
WHOLE: THE SUM OF ITS PARTS
This book is split into four parts.
The first, Part I, provides a little more information about my and others’ research on the whole food, plant-based diet, my reflections on some of the most prominent criticisms this research has received since the publication of The China Study, and more of my own background and journey, as context for understanding where the philosophies in this book have come from.
Part II looks at the reason it’s so hard for so many to not just accept, but even notice, the health implications of this research: the mental prison, or paradigm, in which Western science and medicine operate, which makes it impossible to see the obvious facts that lie outside it. For many reasons, we now operate under a paradigm that looks for truth only in the smallest details, while entirely ignoring the big picture. The popular expression “can’t see the forest for the trees” makes the point well, except that there’s much more at stake here than just trees and forests. Modern science is so detail obsessed that we can’t see the forest for the vascular cambium and secondary phloem and so on. There’s nothing wrong with looking at details (I spent most of my research career doing just that); the trouble occurs when we start denying that there is a big picture and stubbornly insist that the narrow reality we see, heavily laden with our own biases and experiences, is all there is.
The fancy word for this obsession with minutiae is reductionism. And reductionism comes with its own seductive logic, so that people laboring under its spell can’t even see that there’s another way to look at the world. To reductionists, all other worldviews are unscientific, superstitious, sloppy, and not worthy of attention. All evidence gathered by nonreductionist means—presuming that research can get funding in the first place—is ignored or suppressed.
Part III looks at the other side of this equation: the economic forces that reinforce and exploit this paradigm for their own self-interest as they chase financial success. These forces completely manipulate the public conversation about health and nutrition to suit their bottom line. We’ll look at the many ways money affects thousands of small decisions that add up to a big impact on what you, the public, hear (and don’t hear) and thus believe about health and nutrition.
Last, in Part IV, we look at the totality of what’s at stake here and what’s needed if we want things to change.
THE TRUTH BELONGS TO ALL OF US
I wanted to tell this story because I owe it to you, the public. If you are a U.S. taxpayer, you paid for my career in research, teaching, and policy making. I have known too many people, including friends and family, who suffered ill health unnecessarily, just because they did not know what I have come to know—and they also were taxpayers. You have a right to know what your money bought and a right to benefit from its findings.
My own disclaimer: I have no financial interest in your believing me. I don’t sell health products, health seminars, or health coaching. I’m seventy-nine years old, I’ve had a long and rewarding career, and I’m not writing this book to make a buck. When you start talking about what you’ve learned from this book with your friends and you encounter passionate disdain for me and my motives (and you will!), just consider the original source of the claims they’re citing. Ask yourself: What’s their financial interest? What do they have to gain from suppressing the information I share here?
Telling this story has been a challenge. I know well that a diet consisting only of plants sounds like a wacky idea to many folks. But that’s starting to change. This idea becomes bigger and bigger with the passing of time. The current system is unsustainable. The only question is, will we free ourselves before it takes us down with it? Or will we continue to pollute our bodies, our minds, and our planet with the slag of that system until it collapses under its own economic weight and biological logic?
In previous generations, how we ate appeared to be a personal and private matter. Our food choices didn’t seem to contribute much, one way or the other, to the well-being or suffering of other people, let alone animals, plant life, and the carrying capacity of the entire planet. But even if that were ever true, it no longer is. What we eat, individually and collectively, has repercussions far beyond our waistlines and blood pressure readings. No less than our future as a species hangs in the balance.
The choice is ours. My hope is that this book will encourage you to choose wisely—for your health, for the next generations, and for the entire planet.
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Okay, I'm ready to proceed.
Step 2: Summary (in English)
The text is an excerpt from a book critically examining low-carbohydrate diets, arguing they are a "fraud" detrimental to long-term health despite potential short-term weight loss. The author, a nutritional researcher, contends that these diets are appealing due to marketing and a public desperate for weight loss solutions, but their health impacts are negative, often worse than the Standard American Diet they aim to replace. The author contrasts this with the benefits of a Whole Food, Plant-Based (WFPB) diet, which he advocates as optimal for weight management, vibrant health, and longevity. A significant portion of the text is dedicated to deconstructing the arguments of low-carb proponents, particularly Gary Taubes, accusing them of misinterpreting history, misrepresenting scientific evidence (e.g., the definition of "low-fat"), and employing "sleight of hand." The author also criticizes the scientific and medical establishment and food/pharmaceutical industries for obscuring the truth about nutrition due to entrenched paradigms and financial interests. The tone is authoritative, persuasive, and critical, aiming to educate a general audience about what the author believes is the true path to health.
低碳水化合物的騙局
美國人為減重所苦,早已不是秘密。自1980年肥胖問題的攀升首次引起媒體關注以來,全國肥胖率已翻了一倍。如今,超過三分之一的美國成年人屬於肥胖。儘管每年都有數百種新的(或巧妙重新包裝的)「解決方案」以書籍或預製食品的形式上架,我們似乎就是無法遏止這股趨勢。然而,我們國家的體重問題僅是冰山一角;超重與一些導致過早死亡的主要原因有關,包括心臟病、中風、第二型糖尿病和某些癌症。
本書主要探討低碳水化合物飲食——這是眾多解決方案中,在商業上較為成功,卻也對健康最具威脅性的一種,用以滿足我們減重和追求健康的渴望。我們將討論低碳水化合物飲食為何如此誘人、我們如何被誤導以為它有益健康,以及其對健康的真實影響。但本書也關注這些現象背後的營養觀念:碳水化合物有害的觀念從何而來,以及為何儘管有大量相反證據,這種觀念依然存在。
坊間幾乎一直都有各種風靡一時的飲食法,其科學依據各不相同,有些效果較好,有些則不然。數十年前,乃至今日某種程度上,最受信任的建議基本上是:少吃多動。減重被視為一道算術題——攝取的卡路里對比消耗的卡路里。但我們也被告知,膳食脂肪是問題所在。脂肪使我們,嗯,變胖。所以如果想減重,我們只需要減少攝取脂肪即可。
然而,隨著全國肥胖率的上升,顯然這種關於脂肪的建議並不管用。「標準美國飲食」(SAD)也同樣無效。我們需要重新思考我們看待適當營養的方式。正是在1980年代,隨著這些日益增長的擔憂,低碳水化合物運動開始盛行。它在1988年達到巔峰,隨著羅伯特·阿金斯醫生的《新飲食革命》出版而大行其道,這本書之所以「新」,僅因其承襲了阿金斯醫生1972年出版但市場反應平平的《阿金斯醫生飲食革命》。而這本「新」書的內容,代表了一套關於體重、營養和健康的誘人另類信仰體系。
簡而言之,低碳水化合物運動要求追隨者嚴格限制碳水化合物的攝取,轉而從蛋白質和脂肪中獲取絕大部分熱量。書中聲稱,「標準美國飲食」的問題不在於脂肪,而在於碳水化合物——那些存在於麵包、米飯、義大利麵、水果和澱粉類蔬菜中的碳水化合物。阿金斯宣稱,減重的最佳方法是減少碳水化合物的攝取。
而且它確實有效!透過大啖培根、牛排和奶油,低碳水化合物飲食者確實減掉了體重。這本是好事,但有一個重要的問題:低碳水化合物飲食對人體健康並無益處。一份又一份的報告顯示了高蛋白、高脂肪飲食的不良影響。它和它試圖取代的「標準美國飲食」一樣糟糕,甚至更糟。
在本書中,我將探討幾個重要問題:為何人們認為低碳水化合物飲食是個好主意?低碳水化合物熱潮背後的真相為何?真正能達到理想體重,同時獲得健康與長壽的最佳飲食又是什麼?
若說我希望各位能從本書中帶走一件事,那就是:低碳水化合物飲食快速減重的能力,遠遠不及這種以動物性食品為主的飲食所伴隨的嚴重健康問題。
低碳水化合物飲食的誘惑力
我在實驗營養學研究領域投入了四十餘年,先是在維吉 ParkingLot工大學,之後在康乃爾大學,期間持續關注最新發現,並在實驗室和實地進行自己的研究。身為一名營養研究員,我起初對於低碳水化合物飲食的普及和商業成功感到驚訝,尤其考量到其嚴重的缺陷。關於高蛋白、高脂肪飲食的研究一致顯示,它們會對健康造成災難性的影響,並且無法確保飲食的依從性和長期的體重控制。因此,我認為指出一些促成這些飲食之所以吸引人的因素是有益的。
不難想像,無論是當時還是現在,節食者為何會被嘗試截然不同方法的想法所動搖。數以百萬計的美國人正在節食。食品製造商和行銷人員將市場充斥著旨在幫助我們減重並維持體重的食品。電視上不斷播放著資訊型廣告,吹捧著能幫助我們擺脫那些難看贅肉的新奇小玩意、運動常規、藥丸和粉末。然而,顯然地,這些方法似乎都沒用。
要呈現令人震驚的視覺效果,請比較這兩張投影片,它們取自美國疾病管制與預防中心(CDC)的簡報。第一張投影片顯示1990年的數據,遠非理想:
在五十二個州及美國其他行政區中,有四十六個地區的成人肥胖率介於百分之十至百分之二十之間,肥胖的定義是身體質量指數(BMI)大於三十。沒有任何州的肥胖率超過百分之二十。
現在看看2010年的數據:
僅僅二十年後,即使是肥胖率最低的州(低於百分之二十五),其肥胖率也比1990年肥胖率最高的州還要高。更有十二個州突破了百分之三十以上的大關。
2011年的數據尚未納入投影片中,但已新增了一個類別:成人肥胖率達百分之三十五或以上。雖然嚴格來說並無必要新增此類別(阿拉巴馬州以百分之三十四點九的肥胖率最為接近),但美國疾病管制與預防中心顯然是在未雨綢繆。
鑒於龐大的減肥產業及其驚人的無效性,另類方法會受到歡迎是很自然的。低碳水化合物飲食是獲得最廣泛公眾接受,因此也佔有最大市場份額的另類方法。但為何低碳水化合物飲食能勝過其他非傳統方法呢?
其中一個主要答案是行銷話術。在這點上,我不得不佩服羅伯特·阿金斯。我的新書《整體: rethinking the science of nutrition》(2013) 的主要主題之一是,典範,或根深蒂固看待世界的方式,極難改變。但阿金斯和他的支持者們顛覆了長達一世紀的營養學智慧,將膳食脂肪和膽固醇塑造為營養英雄,並攻擊任何指出相反研究結果的人。他們允許美國人大量食用地球上一些最不健康的食物,而且不僅毫無罪惡感,反而帶有自豪和優越感。阿金斯熱潮最令人印象深刻的遺產是一項語言上的成就:創造了「低碳水化合物」一詞,從而將大多數植物性食物——這些食物以前被認為是最健康的飲食選擇——變成了危險且易致胖的禁忌品。
其吸引力顯而易見,原因不言自明。數十年來,人們相信唯有依靠沙拉、令人沮喪的半個葡萄柚加無脂茅屋起司午餐,以及喝起來像電池酸液的減肥汽水,才可能減重。如今,他們卻被告知可以盡情享用自己喜愛的食物:牛排、培根、奶油、豬油、奶油乳酪、橄欖油、美乃滋和雞蛋。飲食再次變得有趣!
而且,瞧!人們發現——在這種飲食的初期階段——他們確實減輕了體重。那些多年來醫生和公職人員一直警告的食物,似乎比那些索然無味、奪走所有飲食樂趣的零脂肪加工食品更能有效地促進體重減輕。
阿金斯飲食法的追隨者不僅能毫無罪惡感地滿足對脂肪和蛋白質的渴望,甚至還能對那些仍在吃沙拉、參加減重會議、計算卡路里的可憐蟲們感到優越。
阿金斯飲食法不僅吸引了節食者,對肉類、乳製品和蛋品產業也是一大福音。這些公司不僅能以低碳水化合物的「科學」來抵擋公眾對其產品的批評,銷售額也因此增加。
低碳水化合物飲食的版圖
當然,並非所有低碳水化合物飲食都是一樣的。阿金斯開創的低碳水化合物宇宙已經擴展到包含許多不同的飲食法和飲食哲學。但這些飲食法之間的區別更多在於行銷手法而非實質內容——它們都同樣恐懼和厭惡碳水化合物,並建議從蛋白質和脂肪中獲取大部分熱量。
阿金斯
雖然羅伯特·阿金斯是現代低碳水化合物運動之父,但他並非低碳水化合物概念的始創者,這一點他在書中坦然承認。有記錄以來第一位使用此類飲食法的人是威廉·班廷,一位1860年代的英國殯葬業者。班廷在六十六歲時,經其醫師威廉·哈維醫生建議,嘗試了低碳水化合物飲食。他在最初幾週體重下降,並表示或許願意繼續這種飲食——儘管據我所知,班廷改變飲食的長期效果從未明確。在接下來的一個世紀裡,另有幾位醫療從業人員曾與其病患嘗試低碳水化合物飲食,但直到1972年阿金斯醫生的《飲食革命》出版,這個概念才進入大眾視野。
乘著低碳水化合物飲食短期成功的浪潮,阿金斯在2003年逝世前撰寫了多本著作。他的專業生涯演變成一個帝國;截至2013年撰寫本文時,1988年出版的《阿金斯醫生新飲食革命》已售出超過一千五百萬冊,而生產和授權阿金斯認可產品的阿金斯營養品公司(Atkins Nutritionals, Inc.)年銷售額達數百萬美元。阿金斯基金會資助低碳水化合物飲食與肥胖、阿茲海默症、攝護腺癌及其他疾病相關的研究。儘管創辦人逝世且公司在2004年至2005年因管理不善而一度破產,阿金斯帝國依然屹立不搖;其現今的業務仍在減重市場佔有重要一席之地。
低碳水化合物飲食的衍生品
嗅到商機,許多其他醫生和作家紛紛為低碳水化合物現象添上自己的色彩,創造出各自的書籍、飲食法和產品。其中最著名的包括瑪莉·丹和麥可·伊德斯的《蛋白質力量》(1995年)、貝瑞·希爾斯的《進入區域》(1995年)、彼得·迪亞達莫的《吃對血型》(1997年)、羅倫·科代恩的《舊石器時代飲食法》(2002年)、亞瑟·阿格斯頓的《南海灘飲食法》(2005年),以及艾瑞克·衛斯曼的《新阿金斯飲食法》(2010年)。如同努力脫穎而出的弟妹一般,這些不同的作者及其支持者們費盡心思區分他們「正確」的飲食法與其他飲食法。《南海灘飲食法》偏好橄欖油而非奶油,並強調較瘦的肉塊。《蛋白質力量》添加大量水分和營養補充品,以彌補低碳水化合物飲食的不足。《進入區域》表面上否定了低碳水化合物的概念,建議蛋白質「僅」佔百分之三十,但仍將碳水化合物限制在總熱量的一半以下。(這仍然是低碳水化合物飲食!)即使是《舊石器時代飲食法》,儘管其正面強調全食物,也只是同樣低碳水化合物、高蛋白、高脂肪概念的另一種版本(見附錄)。這些衍生品都只佔據了人類飲食連續體中極其狹窄的一小部分。
除了對碳水化合物的恐懼之外,這些作者還有另外兩個共通點:缺乏科學研究經驗,以及透過銷售他們的奶昔、粉末、萃取物、油品、能量棒,甚至巧克力所產生的巨額財富,還有透過授權其註冊商標的認可標章所累積的第二筆財富。
所有這些差異化和行銷手法的淨效應,是在文化層面上將低碳水化合物飲食正常化。餐廳例行性地提供低碳水化合物菜單選項。注意體重的人不吃餐前麵包,似乎是理所當然的事。二十年前,如果你為了減重而坐下來享用一頓培根、奶油和牛肉大餐,旁人可能會對你揚起眉毛(並對你的神智產生一些疑慮),但如今,這已是完全正常的減重方法。當荒謬的說法被重複得夠多次,聽起來就像是真理了。
低碳水化合物飲食的真相
如我所提及,低碳水化合物飲食通常在短期減重方面相當有效。但這種益處伴隨著巨大的負面影響。低碳水化合物飲食針對的是過重問題,卻未關注造成體重過重的根本原因,這會導致其他症狀。低碳水化合物飲食往往會使這些其他症狀以及根本原因本身更加惡化。
關注原因與治療症狀之間有何不同?
例如,一片枯黃的草坪是一種症狀。這是一種難看、可能令人尷尬的症狀,可能會讓鄰居們搖頭並在背後議論你。「看他把草坪弄成這樣,」他們可能會咕噥著,「他為什麼不採取些措施呢?」
於是,草坪護理專家帶著解決方案來了:綠色油漆。
瞧——問題解決了!
嗯,不完全是。
將草坪漆成綠色後,它會暫時看起來翠綠,但最終油漆會磨損或被沖刷掉,然後你就得再把草坪油漆工叫回來。油漆對於導致草坪變黃的草的健康狀況不佳,沒有任何改善作用。而且如果油漆有毒,甚至會使草的健康狀況更糟。如果你真的想要一片茂盛翠綠的草坪——一片自然健康的綠色草坪——你需要改善土壤:添加養分、清除毒素、適當澆水,並使用適合你環境的草籽。換句話說,專注於根本原因,而不僅僅是可見的症狀。
如果你想減重,單純專注於減重本身——正如低碳水化合物飲食所做的那樣——就像把草坪漆成綠色一樣徒勞無功。
低碳水化合物飲食的第一個主要缺陷在於其短期性。長期而言,低碳水化合物飲食並未兌現其對節食者的承諾,即幫助他們減輕體重並維持改變。對人群的觀察性研究壓倒性地顯示,反映長期食用動物性及高度加工食品的高蛋白、高脂肪飲食,與更多健康問題相關,其中許多問題與肥胖有關。
儘管現代醫療照護與科技進步,美國人卻越來越胖、越來越不健康。我們在降低癌症、心臟病、中風、糖尿病以及數十種與肥胖密切相關的其他疾病的發病率方面,並未取得任何重大進展。只是,與糖尿病或高血壓不同,肥胖是這個問題更為明顯的表徵。
事實上,肥胖流行病與健康危機是一體之兩面。你無法解決其一而不解決另一。這對個人而言如此,對整個社會亦然。肥胖是一種症狀,就像高血壓、動脈阻塞、心絞痛、慢性呼吸短促、腹痛、頭暈、便秘以及數百種其他症狀一樣。然而,我們卻在很大程度上錯誤地將肥胖視為一件獨立的事情——一種獨立的疾病。
雖然健康的體重與整體健康之間有許多重疊之處,但兩者並非同義詞。罹患癌症可以讓你體重銳減,死亡可以讓你永保苗條,但我可不建議這種方法!寬容地說,我們可以認為低碳水化合物飲食的倡導者是利用減重作為特洛伊木馬,誘使人們改善飲食和整體健康——儘管幾乎沒有證據支持這種慷慨的解讀。阿金斯本人在逝世時既肥胖,又因高蛋白、高脂肪飲食的已知後果而健康狀況不佳,顯然這個社群並未認真看待關於長期健康結果的確鑿數據。
兩篇原創研究論文比其他任何研究都更能揭示阿金斯飲食法的後果,因為它們是由阿金斯飲食法的支持者發表,並由阿金斯組織資助。在一篇論文中,與「低脂」飲食者(其脂肪攝取「僅」佔總熱量的30%)的對照組相比,阿金斯飲食法的使用者遭受更多便秘(68%對35%)、更多頭痛(60%對40%)、更多口臭(38%對8%)、更多肌肉痙攣(35%對7%)、更多腹瀉(23%對7%)、更多全身無力(25%對8%)以及更多皮疹(13%對0%)——即使是那些服用維生素補充劑的阿金斯飲食法使用者也是如此。在另一篇論文中,阿金斯飲食者在便秘(63%)、頭痛(53%)和口臭(51%)方面也出現了類似的盛行率。
這些阿金斯飲食法的副作用具有一致性,且研究結果相當具說服力。也就是說,與本已不良的標準美國飲食(SAD)(其脂肪和蛋白質含量高)相比,脂肪和蛋白質含量更高的阿金斯飲食法,即使在短期內,也會導致更多負面的健康結果。
那麼,為何節食者仍然相信低碳水化合物飲食的誇大宣傳呢?這與低碳水化合物運動的論點聽起來多麼有說服力有很大關係——儘管這些論點一直與科學相矛盾。
蓋瑞·陶布斯與低碳水化合物飲食的障眼法
最佳的謊言往往包含一絲真相,記者蓋瑞·陶布斯的作品尤其如此。他是當今低碳水化合物運動中最能言善道且最具影響力的代言人。陶布斯的兩本暢銷書《好卡路里,壞卡路里》(2007年)和《我們為何發胖》(2011年),以引人入勝且對許多人而言極具說服力的方式,闡述了低碳水化合物飲食的論點。
陶布斯當然並非唯一撰文支持低碳水化合物飲食的人,但我選擇以陶布斯的著作為核心進行批判,因為它們代表了低碳水化合物理念最全面且證據最豐富的表述。陶布斯的作品也不經意地(無疑是如此)概述了低碳水化合物倡導者常見的許多錯誤、邏輯問題和障眼法。透過指出陶布斯的錯誤並揭露其錯誤的推理,我希望能展現整個低碳水化合物運動的失敗和智識上的貧乏。
第一個,或許也是最具 damning 的問題,是對歷史以及所謂低脂飲食與肥胖之間關聯的誤讀。陶布斯在《好卡路里,壞卡路里》一書中探討了這段歷史,該書被譽為對支持低碳水化合物飲食證據感興趣者的必讀之作。雖然陶布斯的敘述確實全面,但他的詮釋,我們可以說,頗具創意。
陶布斯論點正確之處
陶布斯以一絲真相開頭,正確地指出計算卡路里的有效性是一個迷思。他也正確掌握了過去五十年來關於飲食與健康論述的一些重要歷史。在他關於肥胖潛在生化機制的技術性論證中,他也正確掌握了其中一些細節。然而,若孤立看待這些部分真相,並將其編織成關於碳水化合物之害的敘事,最終反而會誤導而非提供資訊。
陶布斯正確地指出,許多早期研究人員在設計研究和報告結果時,混淆了導致肥胖及相關疾病的三個主要假說:過量卡路里、過量脂肪和過量碳水化合物。根據第一個假說——迄今最為普遍的——我們體重增加是因為攝取的卡路里多於消耗的。這就是我先前提到,至今仍常被援引,彷彿是世上最顯而易見之事的假說:「少吃多動。」簡單的算術。值得讚揚的是,陶布斯巧妙地揭穿了這個危險的過度簡化。
陶布斯接著論證,而且是正確地論證,透過控制熱量攝取來創造長期健康是行不通的——這是一個無論專業人士或非專業人士都鮮少理解的重要觀察。大多數人無法長時間維持顯著較低的熱量攝取,即使他們或許能在短期內做到。也就是說,「節食」之所以無效——並非因為我們的意志力不足,而是因為我們的生理上無法健康地維持大幅降低熱量攝取,以顯著減少疾病的形成。無論如何,陶布斯說,通常最重要的並非攝取的熱量多寡,而是熱量在體內代謝和分配的方式(我們將在幾頁後更深入討論)。事實上,陶布斯認為,增加熱量攝取是肥胖的結果,而非原因——我們因其他原因體重增加,然後需要更多熱量來維持該體重。有其他因素導致肥胖,而且是透過決定我們攝取的熱量如何被代謝和利用來達到此目的。
我讚賞陶布斯推翻卡路里假說。事實上,我早就說過,我們不應過度強調「卡路里攝入;卡路里消耗」的假說,或以精確數量描述卡路里,彷彿它們是像分子一樣具有結構和形態的實體,因為這樣做只會賦予它們額外的重要性。
卡路里僅是衡量分子內所含能量的單位,尤其指結合原子的化學鍵中的能量。想像一堆木柴。我們知道那堆木柴裡有能量,但我們看不見也感覺不到。然而,當我們用火柴點燃木柴時,隨著木柴燃燒起來,我們會感覺到能量釋放出來。營養素的卡路里含量也是透過測量營養素燃燒時釋放的熱量來決定的。為了計算這個值,巨量營養素(脂肪、蛋白質和碳水化合物,這些營養素提供了食物絕大部分的重量)在實驗室的受控條件下燃燒,所散發的熱量——溫度的變化——即被測量為卡路里。(我傾向稱此特性為「能量」,但由於「卡路里」一詞廣為人知,在此仍沿用此稱呼。)
要產生體重明顯增減所需的卡路里量非常微小——這個觀念也讓我們忽略了對卡路里的重視。五十卡路里的差異,在一天總食物攝取量中可能難以區分;這相當於平均每天不到一茶匙的油。然而,身體每天多保留五十卡路里,理論上一年就可能導致體重增加或減少五到十磅。問題是,攝取卡路里不等於保留卡路里;保留卡路里並非我們能透過計算來有意識地控制的事情。因此,在這方面,陶布斯是正確的:正如我們在中國的研究結果所證實的,除非極端情況,否則卡路里的攝取或消耗並不重要。
陶布斯錯在哪裡
當陶布斯開始辨識「壞卡路里」的來源時,他的觀點便與證據分道揚鑣了。陶布斯認為,過度攝取提供熱量的碳水化合物(前述三個相互競爭的理論中的第二個)是所有飲食罪惡的根源。在他看來,糖(蔗糖或砂糖)和其他碳水化合物(即精製碳水化合物,如澱粉和果糖)的攝取,是美國乃至世界大部分地區肥胖流行的罪魁禍首。他將碳水化合物攝取量激增歸咎於政府推廣第三個相互競爭的理論:來自脂肪的熱量使我們變胖。在陶布斯看來,政府的低脂政策所引發的對脂肪的恐懼,直接將美國大眾推向高碳水化合物飲食的懷抱,因為它鼓勵用碳水化合物取代脂肪。簡而言之,陶布斯認為問題在於碳水化合物過多,而政府(或他對政府的解讀)則認為問題在於脂肪過多。
陶布斯從歷史和科學的角度論證,過量攝取脂肪無法解釋過去三十年來肥胖率驚人上升的現象,正如政府聲明所暗示的那樣。大多數讀者都熟悉關於食用低脂食品的廣泛建議,以及市場上琳瑯滿目的「低脂」食品。陶布斯提出了一個看似合理的解釋,說明該領域的科學家為何會出錯,部分原因是他們缺乏想像力,部分原因是他們固守一種世界觀,這種世界觀不鼓勵對廣為宣傳的以低脂為重點的假說提出專業挑戰,以免遭到嘲笑甚至危及專業地位。陶布斯說,脂肪,而非碳水化合物,才應該是我們主要的能量來源。他說,脂肪是好的,而不僅僅是被傾倒到身體儲存庫中最終變成脂肪組織的東西。
在進一步討論之前,讓我們先思考一下碳水化合物究竟是什麼,尤其因為陶布斯相當傲慢地抨擊科學家不了解這種營養素的特性。(依我經驗,真正對碳水化合物的定義和意義感到困惑的,反而是像陶布斯這樣的記者、企業行銷人員,甚至一些臨床醫師。)
碳水化合物的多樣性
碳水化合物是一種幾乎只存在於植物中的營養素。它是由簡單到極其複雜的化學分子集合而成。簡單碳水化合物包括單醣(如葡萄糖、果糖、半乳糖、甘露糖等)和雙醣,雙醣是由兩個化學鍵合的單醣組成(如蔗糖[由葡萄糖和果糖組成的食糖]和乳糖[由葡萄糖和半乳糖組成的乳糖])。由三個或更多單醣連接而成的鏈狀聚合物稱為多醣。葡萄糖(與血糖中的分子相同)是多醣鏈中最常見的單醣單位,果糖在某些食物中也幾乎同樣常見。澱粉是馬鈴薯和穀物等食物中的主要多醣,是由葡萄糖分子長鏈組成的網絡。
單醣和雙醣通常被認為是「簡單」碳水化合物,因為它們的分子量小,易溶於水,且容易被消化吸收進入血液。有些人推斷澱粉也是「簡單」的,因為它們也能溶於水(雖然會使其變成凝膠或糊狀),並且在消化過程中容易分解成葡萄糖,然後被吸收到血液中。
其他碳水化合物類型則複雜得多。由單醣鏈形成精密的聚合物網絡,有時還包括胺基酸和類脂肪分子側鏈。這些聚合物網絡展現出多種化學、物理和營養特性。例如,一大群通常被稱為膳食纖維的物質,與它們的簡單碳水化合物表親不同,通常不會在腸道中被消化吸收。儘管如此,這些複雜的、類似纖維的物質仍然參與極其重要的生物活動:它們與腸道微生物相互作用,這些微生物將其分解為對身體其他部分有益的產物,尤其是腸道。事實上,簡單和複雜碳水化合物協同作用時,能提供多種健康益處,包括提供能量。
每當我們在自然界中遇到多樣性時,都不應輕率地將其視為不必要或不幸。碳水化合物消化率和功能的廣泛光譜非常重要:它使身體能夠適應不同的狀況,從需要快速爆發能量到促進腸道中其他營養素的消化和吸收。
的確,蔗糖,構成食糖的簡單雙醣,若單獨攝取可能有害。已知從甘蔗和甜菜中提取並以分離形式添加到其他食物中的蔗糖,幾乎沒有或根本沒有有用的健康價值。高果糖玉米糖漿是另一種近期商業上出現並被利用的簡單單醣。最新研究表明,其影響與蔗糖一樣糟糕,甚至更糟。
為了利用此證據支持低碳水化合物運動,陶布斯玩弄了一點障眼法,其關鍵在於:精製糖有害,因此所有含糖(即碳水化合物)的食物都有害。即使從古典邏輯來看,這也是拙劣的邏輯。我們也可以透過思考植物性食物中發現的另一種碳水化合物——纖維——並比較其在天然狀態下以及經過加工、分離並作為與天然狀態分離的物質食用時的健康效果,來突顯這種推理的缺陷。
膳食纖維是從各種全穀植物中提取出來,以便添加到瑪芬和其他烘焙食品中,稱為「麩皮」。行銷人員隨後宣稱這些烘焙食品具有健康益處,並引用關於纖維益處的研究證據。但是,當麩皮從全穀植物中提取出來,然後添加到像麵包和早餐穀物這樣的加工和零碎食品中時,對我們並無幫助。儘管有一些證據表明麩皮補充劑可能會降低某些嚴重健康問題的指標,但我找不到任何證據表明,長期來看,這 tatsächlich 是一種預防或治療這些問題的好選擇。
含有多種複雜形式膳食纖維的全食物,與較低的結腸癌發生率、較低的血液膽固醇以及較低的誘發乳癌的雌激素水平相關。使用從這些食物中分離出來的麩皮,更多的是行銷手法而非為了健康。這對許多分離出來的營養素都適用,它們要麼沒有積極的健康益處,要麼實際上會導致有害影響。
如果陶布斯和他的低碳水化合物同伴反對攝取精煉(即提取)糖,他們就應該明說,而我會是首批支持他們從我們的飲食中消除這些糖的人之一。但是,他們卻將所有碳水化合物都一概而論,這是一種智識上膚淺且不誠實的舉動。(陶布斯比其他一些低碳水化合物的啦啦隊長更為謹慎,但並非完全如此。他應該主動強調這種差異,而不是讓它在公眾論述中潛伏。)
由於水果、蔬菜和全穀物都富含碳水化合物,將所有碳水化合物一概視為不健康,意味著也將植物性食物和單醣妖魔化。低碳水化合物飲食不可避免地是高脂肪飲食,尤其是飽和脂肪,因為消除碳水化合物意味著依賴大量動物性產品來獲取能量和其他營養益處。因此,幾乎可以定義為,低碳水化合物飲食強調食用動物性食物,而低脂飲食則強調食用植物性食物。依我經驗,低碳水化合物(因此也是高蛋白、高脂肪)飲食中對動物性食物的這種強調,正是低碳水化合物倡導者的主要動機。
陶布斯對碳水化合物定義與意義的過度簡化所建議的飲食消耗劇烈轉變,將產生重大後果。轉向低碳水化合物飲食不僅嚴重減少我們對抗氧化劑、複合碳水化合物、維生素和某些礦物質的攝取,同時也將我們的膳食能量來源從碳水化合物轉向脂肪,並鼓勵攝取遠高於所需量的蛋白質。
為何這如此糟糕?因為我們選擇用來滿足能量需求的食物,對於我們是體驗健康還是疾病,有著天壤之別。
卡路里數量與卡路里來源
如果陶布斯所謂的「好卡路里與壞卡路里」指的是「好的與壞的能量來源」——實際上是好的與壞的食物——那麼至少在原則上,我與他意見一致。植物性與動物性食物在營養成分方面有極大差異,注意你攝取的食物種類遠比執著於計算卡路里,而不考慮這些卡路里來源重要得多。
舉例來說,我們針對膳食蛋白質對實驗動物癌症生長影響的研究,包含了約三十年來進行的大約二十五項獨立實驗。攝取最低蛋白質含量(佔總熱量5%)的動物,其癌症發生率遠低於攝取較高蛋白質的同類,儘管它們平均多攝取了2%至3%的總熱量(或者,我更傾向於說,更多的總能量)。這是一個重要的觀察:攝取更多熱量,但癌症卻更少。
要說服我的一些同事接受這個發現並不容易,因為他們長期以來幾乎堅信我們的結論應該完全相反:增加卡路里會導致癌症(以及其他疾病)的發生率增加。這些關於卡路里與癌症關聯的信念,是基於先前的實驗研究,這些研究顯示當卡路里攝取量大幅減少20%至30%或更多時,癌症發生率會降低。
我們發現攝取更多卡路里也可能意味著更少癌症,這起初也讓我們感到困惑。透過額外的研究,我們了解到,這個結果的原因是膳食蛋白質對身體能量分配和利用的影響。低蛋白飲食(例如全食物、植物性飲食)會增加膳食卡路里以體熱形式消耗的比例,或透過自主體能活動消耗的比例,從而避免將這些能量儲存為體脂肪。我們實驗中低蛋白組的動物消耗更多氧氣,並形成更多高度特化的組織(稱為棕色脂肪組織),這種組織將卡路里/能量從體脂肪的生成中轉移出去,轉而用於產生體熱,這個過程有時被稱為代謝性產熱。簡而言之,低蛋白飲食產生的兩個過程——增加產熱作用和增加體能活動——都將卡路里從體脂肪的生成中轉移出去。在這些及其他研究中,對體重增減至關重要的關鍵差異在於身體如何利用卡路里,而非攝取的卡路里量。
這不僅發生在老鼠身上;這些實驗室動物研究的結果與我們對中國農村人口的觀察結果一致。中國每單位體重的卡路里消耗量顯著高於西方人,然而中國的身體質量指數(BMI)卻大幅較低。
用通俗的語言來說,研究中的中國人攝取更多卡路里,但體重卻較輕——即使在補償了他們較大的體力活動量之後也是如此。和我們的實驗動物一樣,這些人吃的是低蛋白(但碳水化合物含量極高!)的飲食,幾乎所有蛋白質都來自植物性食物。根據一群英國研究人員先前的發現,有理由認為這些人在體力活動期間將攝取的卡路里轉化為體熱,就像我們的實驗動物一樣。(我認為這有點像吃完高脂、高蛋白餐後產生的遲鈍感,相對於低蛋白、低脂餐後的精力充沛「輕盈」感。)此外,請記住,即使身體卡路里分配的微小變化(每天50卡路里),一年內也可能對體重產生重要影響。
那麼,我們在中國的研究結果顯示,攝取全食物、植物性、高碳水化合物的飲食(其中75%至80%的總能量來自植物)可以透過將能量分配轉向體力活動和產生體熱,而非長期儲存為脂肪,來最大限度地減少體重增加。事實證明,體重增加與我們攝取的卡路里數量幾乎沒有關係,而完全與這些卡路里在體內的使用方式有關。
研究(脫離)脈絡
這些時而令人困惑、具挑釁性且難以理解的發現,應當引發對證據可靠性的質疑。陶布斯引用了數百項研究來「證明」他的理論。但我堅持認為,他的結論——主要是低脂飲食使人發胖——顯然無論從歷史還是科學證據來看都站不住腳。我為何能這麼說?這個問題的答案在於對研究通常如何進行,以及科學家(在此特指陶布斯和我)如何詮釋研究結果的考量。
陶布斯利用極其複雜證據體系中狹隘定義研究的證據,創造出他自己的一套新敘事。當像這樣的孤立事實被編織在一起時,敘事受到個人偏見影響的風險更高,尤其當最終成品未經專業評估和審查,或未獲其支持時。而陶布斯的作品從未經過專業、合格同行的評估。
就陶布斯而言,還有更多需要考量之處:他引用的研究報告沒有一項是他自己的。他並非科學家,也未曾進行過任何自己的實驗研究。所有這些都增加了他從這些零散細節中建構的敘事受到其既有偏見影響的可能性。雖然研究科學家並非不受偏見影響(事實上,正如我在《整體》一書中所描述的,某些類型的偏見在科學界普遍存在),但他們必須面對自己研究結果的事實,並且不能假裝忽略它們,這在某種程度上限制了他們像陶布斯那樣「斷章取義」的餘地。
陶布斯選擇納入哪些證據的方式,有點像檢察官獨攬陪審團遴選權的結果。陪審員可能都是可敬的公民,但他們幾乎肯定只代表總人口中的特定一部分,其特質和觀點會偏向檢方。
因此,陶布斯引用的每一篇論文,都應根據若干重要議題進行仔細審視:
♦ 可能影響論文結果的眾多實驗因素與條件;
♦ 實驗研究設計的適切性;
♦ 統計顯著性水平;
♦ 不僅是每項特定研究,也包括其作者們的資金來源;
♦ 期刊的專業聲譽;以及
♦ 解釋數據所使用的方法。
這些問題對大多數讀者而言並不容易評估,他們很可能不熟悉科學研究的規範。事實上,即使對經驗豐富的研究人員來說,這些問題也未必容易評估,尤其是當研究人員並非在該研究領域的直接工作者時。
我承認,我並未取得陶布斯所有參考文獻以進行我自己的批判性審查和詮釋——這項任務因其繁瑣且有問題的引用方法而變得異常困難。因此,為求權宜,我選擇給予陶布斯方便,直接接受他認為支持低碳水化合物飲食健康價值的證據(通常是間接證據)(例如較低的體重、較低的糖尿病發生率等)。
然而,即使我們假設證據同樣有效,問題依然存在:為了解釋支持低碳水化合物飲食的研究結果——在最初遵循低碳水化合物飲食與標準美國飲食(SAD)相比時,體重、血脂,以及重要的是循環胰島素的降低——陶布斯必須將一些細節編織在一起,這些細節雖然個別來看可能健全,但卻無法準確描述整體的功能。
首先,我們需要檢視陶布斯在這些結論中使用的一些基本概念——關於身體在碳水化合物方面的功能細節,這些細節普遍被認為是正確的,但事實上遠非如此。儘管陶布斯的出發點是正確的,但他對能量產生和新陳代謝結果的看法非常狹隘,因為它與體內無數其他事件相互作用。
當攝取碳水化合物且食物在腸道消化後,會產生葡萄糖。這種葡萄糖被吸收到血液中,然後在胰島素的協助下進入細胞,在那裡被氧化產生能量。這滿足了我們的飢餓感——細胞產生的能量需求,並轉化為我們想吃食物的慾望。
未立即用於產生能量的葡萄糖,可能以肝醣(一種澱粉狀多醣)的形式儲存在肝臟和肌肉中;當需要能量時,細胞也能相當快地利用它。未使用的葡萄糖還有第二個選擇:它可以轉化為三酸甘油酯(脂肪),這是一種更穩定的能量儲存形式,逐漸累積形成脂肪組織,也就是肥胖的元兇。
進食後,身體的血糖濃度會上升,然後在幾小時內隨著葡萄糖被細胞用來提供即時能量或轉化儲存而回到基準線。由於進入血液的葡萄糖會自動觸發胰島素釋放,因此隨著我們間歇性進食,血糖和胰島素的血液濃度會一起波動。所有這些對健康的人來說都是非常正常的過程。
然而,對太多人而言,高精緻碳水化合物和單醣的飲食會導致血液中葡萄糖濃度持續偏高。為了代償,這些高葡萄糖濃度需要持續高水平的胰島素,而這種胰島素由於某些未知原因,會逐漸失去促進葡萄糖進入細胞的能力。為了克服這種減弱的胰島素活性——或稱「胰島素阻抗」——胰臟會分泌更多胰島素來應對,從而形成一個具有不良後果的惡性循環。較高的血糖濃度導致釋放更多胰島素,如果這種狀態持續過久,會導致更嚴重的胰島素阻抗,進而導致更高的血糖濃度。因此,我們可以將這個循環的影響視為一種胰島素過剩的疾病,或者,如在第二型糖尿病、肥胖和心臟病中所見,是一種葡萄糖毒性。根據陶布斯的說法,發生這種情況的原因是經常性地過量攝取碳水化合物。
胰島素除了協助葡萄糖進入細胞及代謝外,還有許多其他正常功能。它也可能協助葡萄糖以三酸甘油酯(脂肪)的形式被吸收、代謝和儲存。雖然這種儲存的脂肪可以被重新提取並代謝以產生能量,但血液中高濃度的胰島素傾向於阻止這種儲存脂肪轉化回能量的過程。因此,過量的胰島素會使身體其他部位的細胞渴望能量。作為回應,我們繼續進食——並繼續增加體重,因為身體儲存了更多葡萄糖。
根據陶布斯的說法,解決血液中胰島素過多這個問題最實際的方法,就是不要讓高葡萄糖食物,尤其是那些容易消化吸收並經常產生脂肪的精緻碳水化合物,大量湧入系統,藉此減少對胰島素的需求。
即使僅從表面看,這其中也有一些問題。雖然關於碳水化合物消化、吸收和利用的這些基本原理大致正確,但應注意的是,它主要指的是精緻碳水化合物的影響,而非存在於全食物中的總碳水化合物。此外,短期、脫離脈絡的發現——可以說是試管中的發現——必須與長期健康結果相符。有許多例子顯示,實驗室中脫離脈絡的發現並不等同於真實生活經驗。(也許其中一個較為人知的例子是關於抗氧化劑β-胡蘿蔔素,維生素A的正確形式,當它存在於食物中時與健康的反應相關,但當作為補充劑食用時則會導致不健康的反應。)
我再重複一次:根據目前科學知識,陶布斯在此所說的部分內容確實準確,他用來建構這個故事的發現也可能代表了高品質的研究。但故事本身,以及他得出的解決方案(低碳水化合物飲食),卻並非事實;許多其他研究的證據顯示,高碳水化合物飲食,如全食物、植物性飲食,也能產生脂肪分解和體脂減少。陶布斯使用的研究發現指的是已從其自然環境中分離出來的事件。
將孤立的事件組合成一個連貫的故事,只有當拼圖的各個部分都放在正確的位置時才能成功。可悲的是,同樣的過程也可能輕易地被用來證明實際上是錯誤的事情。例如,如果我們想證明可口可樂促進健康,我們可以設計一項研究,讓一些人喝可口可樂,而另一些人則完全不喝任何液體——並且從不比較可口可樂與水的影響。這幾乎是所有飲食與健康研究的困境:我們是否擁有足夠或正確種類的細節,來可靠地建立一個真正有效的假說。
我並非暗示所有著眼於特定細節的研究(本質上具有典型還原論特徵的研究)都是刻意帶有偏見或毫無價值的。精心建構的還原論研究可以透過提供解釋——特定的細節和機制——來加深我們對人類健康整體的理解,這些解釋能穩定並支持整體論研究:這種研究不僅審視單一研究的證據,更審視目前所有可得的證據,並據此得出結論。還原論研究必須服務於只能從整體觀照現實才能獲得的「宏觀」真理。這對於營養學研究尤其如此。
一個經典的比喻,我在《整體》一書中詳細探討過,就是那個古老的故事:六個盲人被要求描述大象。一個人摸到象鼻,說大象像水管。另一個人摸到象牙,說像長矛,第三個人摸到象腿,說像柱子,以此類推。他們所有的探索都有其價值,但每個人的結論都導致對他們被要求描述之物的錯誤理解。只有當出發點是對整隻大象的理解時,我們才能理解那些零散的發現。
任何僅著眼於單一疾病、單一營養素或單一脫離脈絡族群,且與所有整體證據相矛盾的研究,本身都不能被視為證據。當還原論的發現與宏觀圖景相矛盾時,拆毀宏觀圖景是沒有意義的。相反地,我們尋找例外、細微差異和更深入的理解——尋找將異常數據點與已證實的現實相協調的方法。有時,當我們重複實驗卻無法複製結果時,會發現相互衝突的細節只是偶然現象(統計不確定性的隨機結果)。有時,我們會發現實驗本身的前提就有缺陷。
鮮少有無法解釋的數據點能推翻整個思想體系,儘管偶爾確實會發生;我們稱這種現象為典範轉移。例如,哥白尼和伽利略發現了異常數據,最終推翻了自古以來普遍認知的以地球為中心的宇宙體系。但我們不能僅憑單一與現有理論相衝突的還原論發現,就草率地宣佈該理論無效。異常和矛盾的數據必須受到尊重,但我們尊重它們的方式是透過嚴謹地追尋真理,而不是僅僅因為這樣做能增加我們的財富或滿足我們的自負,就將其提升為教條。
這基本上就是低碳水化合物倡導者正在做的事。他們忽略了全面描述整體情況的發現,反而將異常或矛盾的數據奉為圭臬。
低脂飲食究竟有多「低脂」?
陶布斯在另一個重要方面也犯了錯誤,這與未能明確定義「低脂」一詞有關。事實上,低碳水化合物倡導者對「低脂」一詞的濫用,是他們整個敘事中最令人髮指的曲解之一。
低碳水化合物倡導者支持低碳水化合物(但高脂肪!)飲食的論點,建立在他們錯誤的觀念之上,即認為增加膳食脂肪並不重要——節食者多年來一直努力遵循政府的低脂建議,然而沒有人變得更瘦或更健康。事實上,低碳水化合物倡導者聲稱,這些政府推薦的低脂飲食實際上導致了肥胖。
這些聲明基於一個假設,即那些「低脂」飲食者實際上遵循的是低脂飲食。但事實並非如此。這是一個迷思。這種所謂的低脂飲食,脂肪含量一點也不低。
根據陶布斯在《好卡路里,壞卡路里》一書中的說法,將國家天平傾向低脂飲食的轉折點,是明尼蘇達大學教授安塞爾·基斯在1950年代發表的關於膳食脂肪與心臟病關聯的研究。基斯在此項研究之前已是知名的營養權威;第二次世界大戰的K口糧便是由他配製並以他命名。他也以其「飢餓研究」聞名,在該研究中,他讓出於良知反對服役的志願者處於近乎飢餓的狀態,以探究營養剝奪對人體生理的影響。
基斯在戰後開始他的研究,起因於一項異常的發現:明尼蘇達州最富有的商人,他們理應能負擔最好的食物和醫療保健,卻不成比例地承受著較高的心臟病發病率。基斯所有的學術追求都圍繞著飢餓以及士兵在戰鬥條件下所需的最低熱量,因此你可以想像,當他發現過量攝取當時(且至今仍被大多數人認為是)最高品質食物的豐富動物性食品,似乎使男性健康狀況更差而非更好時,他有多麼驚訝。
基斯後續的研究指出,高總脂肪飲食,尤其是飽和脂肪和膽固醇含量高的飲食,與心臟病之間存在關聯。他最初的研究對象是明尼蘇達州的商人,後來將研究範圍擴大到世界四個地區的七個國家。這項名為「七國研究」的成果,於1970年以文章形式發表,並於1980年出版成書,在關心國家健康政策的公職人員和政治人物中引起軒然大波。在後續的研究中,基斯擴大了研究範圍,發現膳食脂肪對肥胖、糖尿病和癌症也有類似的影響。
根據基斯的說法,高脂飲食之所以會促進這些疾病,可以解釋為脂肪每公克含9大卡,屬於熱量密集型,而碳水化合物和蛋白質則為每公克4大卡。因此,高脂飲食意味著熱量密集型飲食和更高的熱量攝取。這是一種將當時流行的兩種觀點——即熱量和脂肪各自都會增加肥胖和與肥胖相關的疾病——巧妙地結合在一起的方式。
基斯對脂肪,尤其是飽和脂肪和膽固醇的關注,意味著應限制富含這些營養素的食物,特別是肉類和蛋類的攝取。其研究的廣泛普及也導致市場上牛奶的脂肪含量從全脂轉向低脂甚至脫脂。(在我長大的乳牛場,我們重視牛奶的乳脂含量,無論是在成品牛奶的定價,還是在旨在培育能生產高脂牛奶後代的育種計畫中。我記得當我們在農場上聽說公眾輿論開始轉向不偏好高脂牛奶時,正是安塞爾·基斯的研究結果導致了這種轉變。)
基斯積極推廣其研究成果,除了學術著作外,還與妻子瑪格麗特合著了兩本暢銷飲食書籍:《吃得好,保健康》(1963年)和《如何健康飲食:地中海方式》(1975年)。基斯的一個典型觀點是:北美洲人「把胃當成了處理一長串有害食物的垃圾處理器」。
我有幸兩次見到基斯:一次是他在康乃爾大學演講,當時我還是研究生;另一次則晚得多,當時九十多歲的基斯出席了我在哈佛大學就我在中國的研究成果所作的演講。基斯對營養學領域的最終貢獻,或許是他「言行一致」所樹立的榜樣——他於2004年逝世,距離他101歲生日僅差兩個月!
陶布斯聲稱,基斯比任何其他作家或研究人員都更能將公眾的注意力集中在膳食脂肪是導致肥胖和健康不佳的主要元兇上。根據陶布斯的說法,美國政府基於基斯研究制定的政策不僅未能改善我們的健康,反而造成了它試圖預防的流行病(肥胖、心血管疾病、糖尿病)。
這種詮釋在兩個層面上都是不正確的。首先,陶布斯假設基斯提倡降低飽和脂肪和膽固醇的攝取量,作為減少心臟病的唯一策略。雖然這部分正確,但基斯也關注這些營養素的來源:即動物性食物。例如,他在討論以人口為基礎的研究中飽和脂肪與血清膽固醇的高度相關性,以及這對「乳製品和肉類產業造成的困擾」時寫道,這些產業的「產品佔了英國和美國幾乎所有的飽和脂肪,以及大多數其他國家的飽和脂肪。」其次,據我所知,基斯從未真正以脂肪佔熱量理想百分比來定義他推薦的「低脂飲食」;他認為依賴政策制定者設定的特定基準並不合理。
換句話說,陶布斯雖然掌握了部分細節,卻因錯誤呈現低脂飲食的定義及其所謂的健康影響,而忽略了這段歷史的細微之處。
聯邦資助報告中(其中一份由我共同撰寫,遺憾的是,我未能如願對其建議施加足夠影響)所提倡的膳食脂肪最低水平是每日熱量的30%。無論如何都不能將此視為「低脂」。1999年的一項全國調查顯示,平均膳食脂肪攝取量從未降至此水平,充其量約為總熱量的33%。認為政府建議將膳食脂肪降至30%或更低曾經達到,或者這樣的水平足以顯示疾病減少,簡直是荒謬。這就好比告訴吸菸者將每天五包菸減少到四包半——然後,在看不到任何效果後,聲稱減少吸菸沒有區別,不值得追求。
不僅這份報告和其他來源的「低脂」建議從未被聽取,脂肪的絕對攝取量也並未減少。作為一個國家,我們或許曾對低脂飲食抱持過幻想,但從未真正成功遵循這些建議。儘管過去幾十年來,我們膳食脂肪的百分比可能有所降低(儘管緩慢),但由於我們的總食物攝取量(和卡路里)有所增加,膳食脂肪的消耗量即使沒有增加,也至少持平。聲稱我們遵守了那30%的建議,並且這樣做之後未能達到預期的健康效果,根本是幻想。陶布斯及其擁護者認為低脂飲食未能減少肥胖,甚至可能導致肥胖的論點,是一種稻草人謬誤。
公平地說,從1950年代到1970年代,科學界和健康界確實高度關注脂肪的危害。但他和其他低碳水化合物倡導者卻低估了這種對脂肪關注的轉變,無論是在健康界還是在公共政策中,這種轉變始於1977年的麥高文委員會和1982年關於飲食、營養和癌症的報告(我前面提到的那份報告,其中提出了脂肪熱量佔比的最低建議)。在那份報告中,我們指出脂肪並非癌症和其他疾病的主要原因,而是(天然低脂的)植物性食物與(天然高脂的)動物性食物在飲食中所佔比例的一個標記。換句話說,真正低脂的飲食(例如,熱量10%來自脂肪)根據定義就是一種富含優質全食物(非加工)植物性食物,且動物性食物含量低的飲食。
麥高文報告關於膳食脂肪的建議,其用意是在整體目標的脈絡下理解:增加植物性食物的攝取,同時減少動物性食物的攝取。我確信陶布斯知道這一點;報告中明確指出,尤其是在關於肉類攝取的評論中。然而,他仍然將論點集中在膳食脂肪和(被錯誤標籤的)低脂飲食的失敗上,卻忽略了主要問題:動物性和植物性食物的平衡。
麥高文報告
讓我們仔細審視麥高文委員會關於膳食脂肪與心臟病關聯報告的歷史:它真正說了什麼,以及它真正產生了什麼影響。麥高文這個高度政治化的委員會最初成立於1970年代初期,在他競選總統失敗後,以及他參觀了普里蒂金健康診所之後。在那裡,他親眼目睹了與他及大多數美國人所遵循的飲食截然不同的飲食所帶來的顯著健康益處:一種真正低脂且富含全植物性食物的飲食。在邀請專家作證後,麥高文委員會建議減少膳食脂肪,尤其是飽和脂肪和膽固醇的攝取,正如基斯和其他研究人員所建議的那樣。由於這種脂肪在動物性食物中含量遠為豐富,因此麥高文委員會建議減少肉類以及「奶油脂肪、雞蛋和其他膽固醇來源」的攝取。不幸的是,市場並未透過改變植物性和動物性食物的比例來回應。相反地,政治家、行銷人員和消費者都特別且不準確地關注於改變他們的脂肪攝取量。
麥高文委員會於1976年提出的一項初步建議,即全面減少肉類消費,在政界和選民中引起軒然大波。結果,該委員會於1977年修訂其報告,建議減少紅肉消費,但不包括魚類和雞肉等白肉——這是一個政治決定,而非科學決定。然而,即使這樣也未能達成足夠的政治妥協。麥高文親自告訴我,幾位著名的中西部參議員隨後在1980年的選舉中落敗,因為他們支持其委員會的建議,激怒了他們的政治基礎——畜牧業農民。從哈佛大學休假並擔任麥高文委員會工作人員全職專家顧問的馬克·赫格斯泰德教授,告訴我幾個關於某些團體對這些以植物為主的建議做出極端敵對反應的故事。儘管麥高文報告僅涉及飲食對心血管疾病的影響,但公眾的憤怒——或者至少是遊說團體的憤怒——卻異常激烈。我記得當時在想,如果對飲食對癌症(這種更令人恐懼的疾病)的影響也給予類似的關注,可能會產生何種不良反應。
此後不久,美國參議院一個委員會也產生了同樣的疑問。他們組織了一場公開聽證會,並要求國家癌症研究所(NCI)所長文斯·德維塔作證。在作證期間,德維塔表示,他無法確定麥高文委員會關於飲食對心臟病影響的建議是否同樣適用於飲食對癌症的影響。聽聞此言,參議院委員會撥款約一百萬美元給國家癌症研究所,以便在國家科學院(NAS)組織一個專家委員會,審查該主題的現有文獻。我與其他十二人受邀加入這個委員會,該委員會最終於1982年發表了具有里程碑意義的國家科學院關於飲食、營養與癌症的報告。儘管我們建議將膳食脂肪降至總膳食熱量的30%或以下——與麥高文報告中關於心臟病的水平相似——我們也建議(作為一個目標,而非更積極的「建議」)增加水果、蔬菜和穀物等全食物的攝取。
正如預期,這份報告的發布助長了公眾對食物與健康的討論熱潮。根據美國國家科學院的說法,這是他們歷史上最受歡迎的報告。我曾登上公共電視網節目《麥克尼爾-萊勒新聞一小時》,並被《時人》雜誌等多家雜誌專題報導,討論這份報告。而且,如同麥高文委員會報告一樣,政治上的反響也相當激烈。農業界一個著名的特別工作小組——農業科學與技術委員會(CAST)——迅速做出回應;在兩週內,他們就發表了一份對我們報告極具批判性的評論,並將其副本放在每一位國會議員和參議員的辦公桌上。我們當中有些人曾就此向國會委員會作證。
我們在美國國家科學院報告中設定的目標(而非建議)是將膳食脂肪降至30%或以下,這不僅僅是試圖模仿麥高文委員會類似的建議。其目的是強調我們當時根據現有證據認為值得為控制癌症而推行的飲食改變。我們在執行摘要中指出,關於癌症的證據表明,理想的飲食中總脂肪含量應遠低於我們30%的目標——或許是熱量的20%或更低——這將更加強調天然低脂的全植物性食物。我們選擇了30%這個武斷且較為保守的基準,是因為若訂得更低,可能暗示蛋白質攝取量減少,尤其是動物性蛋白質,而當時的政治人物和現在一樣,對乳製品和畜牧業組織的利益非常敏感。
百分之三十的膳食脂肪目標並非意在單獨挑出脂肪或任何其他營養素作為癌症的特定且唯一的飲食影響因素。該報告大力強調攝取全食物,尤其是水果、蔬菜和穀物。如此一來,我們明確指出,我們的任何具體目標均不適用於個別營養素,例如以補充劑形式添加個別微量營養素或減少脂肪。
然而,隨著市場事件的發展,人們開始高度關注個別營養素,例如脂肪(少吃)、纖維(多吃)以及維生素和礦物質(服用補充劑)。這些以及其他類似的回應,一直是我對於科學如何被詮釋並傳達給大眾感到最沮喪的原因之一。似乎每當討論到全植物性食物時,話題總會以某種方式轉向對單一營養素的利用,無論是脂肪、碳水化合物、蛋白質,還是維生素和礦物質補充劑。那裡曾經是,現在依然是金錢的所在。
儘管如此,在1980年代和1990年代,受人尊敬的機構仍持續發表增加植物性食物攝取的建議, culminating in the 1997 World Cancer Research Fund/American Institute for Cancer Research report, which I co-chaired. The first recommendation of this 1997 report bluntly stated: “Consume a plant-based diet.”
在《好卡路里,壞卡路里》一書中,陶布斯嚴重簡化並扭曲了飲食與健康領域的歷史。他使其看起來彷彿整個領域只關注膳食脂肪是一種有害的營養素,而且,科學家們認為30%的脂肪攝取量已足夠「低」。然而,從1970年代到1990年代這段期間浮現的最重要訊息是增加全植物性食物的攝取,並由此推論,減少動物性食物的攝取。
不幸的是,陶布斯並非唯一錯失此訊息的人;大多數公眾也是如此。
理想體重、活力健康與長壽的最佳人類飲食
優良的科學告訴我們,最佳的飲食方式是我所謂的「全食物蔬食」(Whole Food, Plant-Based,簡稱WFPB)飲食。早在我思考實驗室本身的實驗結果之前,證據就已清楚表明這一點。數十年前,每個人都經常被含糊地建議「多吃水果和蔬菜」。但這可能是你第一次接觸到如此多關於WFPB飲食顯著促進健康效果的證據。這並非因為這個想法「邊緣」或證據薄弱;而是因為食品、醫療和製藥產業,如果我們的社會了解到全食物蔬食的健康益處以及動物性及高度加工食品的致病特性,將會損失慘重。證據清楚地指向WFPB飲食是最能可靠地帶來光彩照人的長期健康,以及我們渴望的苗條身材的飲食方式。
首先,一個定義。全食物蔬食(WFPB)飲食由全食物構成——也就是盡可能接近其天然狀態的食物。各種水果、蔬菜、穀物、堅果和種子構成了飲食的主體。它不含任何精製產品,如白糖或白麵粉;不含添加劑、防腐劑或其他我們的身體從未被設計來辨識或消化的化學混合物;不含精製脂肪,包括橄欖油或椰子油;並且盡可能減少——或者更好的是,完全不——攝取動物性產品,最多可能佔總熱量的0%到5%。
透過攝取多樣化的植物性食物,我們其實不必擔心卡路里、碳水化合物、脂肪、蛋白質,甚至維生素的具體含量;這些數字或多或少會自行調節。由於植物性食物主要以碳水化合物為基礎,熱量百分比往往接近碳水化合物佔80%,蛋白質佔10%,脂肪佔10%。當然,如果你持續大量食用酪梨和堅果,並避免綠葉蔬菜,你可能會扭曲這種飲食的精神。但即使你盡最大努力,也很難透過WFPB飲食使蛋白質佔總熱量的比例達到15%。
您是否可以僅增加動物來源蛋白質的總攝取量,同時仍獲得 WFPB 飲食的預期益處?是的,但是從植物蛋白中獲取 15% 的熱量與從動物蛋白中獲取 15% 的熱量並不相同,至少部分原因是這種改變會對伴隨動物性食物的其他營養素的攝取產生重大差異。
在我的第一本書《救命飲食:越營養,越危險?!中國營養研究史無前例的驚人發現》(2004年),與我兒子湯姆合著,我分享了我的實驗室和許多其他科學家累積的研究成果,以證明全食物蔬食(WFPB)飲食的卓越健康效果。在我的第二本書《整體: rethinking the science of nutrition》中,我討論了為何這些證據比那些據稱支持高動物性食物飲食的科學更為可靠和準確。欲知完整故事,我推薦閱讀這兩本書。為配合本文目的,我將提供簡要版本。
正如《救命飲食》所總結的,全食物蔬食(WFPB)飲食提供了異常豐富的抗氧化劑、複合碳水化合物,以及最佳攝取量的脂肪、蛋白質、維生素和礦物質,其中許多都有助於預防疾病。任何偏離此模式的行為——例如食用動物性或加工食品——都會使您錯失這些維持生命營養素的巨大益處。在大多數情況下,補充或強化個別營養素或其組合,都無法恢復全食物對健康的益處。
此外,對本書而言非常重要的一點是,「高碳水化合物」的全食物蔬食(WFPB)飲食能降低與肥胖相關的退化性疾病風險——這與陶布斯大幅減少碳水化合物攝取模型所預測的結果直接相反。
對血糖的影響:全食物蔬食飲食與低碳水化合物飲食之比較
您或許還記得,陶布斯的模型指出,低碳水化合物、高動物蛋白的飲食會降低血糖、胰島素和膽固醇,從而降低肥胖、糖尿病和心臟病的風險。但許多報告以不同方式顯示,事實恰恰相反。
我的朋友大衛·克里切夫斯基,在他去世前可能是這個領域的頂尖研究員,發現「對兔子而言,動物性蛋白質比植物性蛋白質更容易導致高膽固醇血症(血液中膽固醇升高)和動脈粥樣硬化(導致心臟病)」,他引用了幾項研究——這種蛋白質種類的區別,早在六十多年前就首次在動脈粥樣硬化方面被注意到。他也發現這對人類同樣適用。我們在實驗室對大鼠進行的實驗性癌症研究中,比較大豆蛋白和酪蛋白(牛奶中的主要蛋白質)時,也觀察到類似的區別。
同樣地,動物性與植物性蛋白質對胰島素有完全不同的影響。羅馬琳達醫學院的理查·哈伯德博士及其同事艾伯特·桑切斯,針對植物性與動物性蛋白質的影響進行了重要研究,其發現直接關係到陶布斯的模型。根據他們的研究,植物性蛋白質實際上會降低胰島素並增加升糖素(胰島素的拮抗劑),從而預防或逆轉糖尿病。較高的植物性蛋白質/動物性蛋白質比例會抑制脂肪(三酸甘油酯)的形成,同時降低膽固醇合成中關鍵酶的活性。簡而言之,在以植物性蛋白質為主的飲食中(如全食物蔬食飲食——但重要的是,這不適用於高精緻碳水化合物的飲食)普遍觀察到的持續低胰島素水平,與持續低的血液膽固醇水平以及其他疾病(如心臟病、肥胖、多種癌症和其他嚴重疾病)的生物標記物相關,這些疾病在人群中常同時出現。
這意味著高碳水化合物、以植物蛋白為基礎的全食物蔬食飲食(WFPB diet)的表現,與陶布斯預測的完全相反。陶布斯說,高碳水化合物飲食會增加胰島素,將高血糖轉化為脂肪,然後抑制脂肪轉化回能量,使脂肪儲存在細胞中——這就是人們發胖並最終罹患糖尿病和其他與肥胖相關疾病的原因。雖然這聽起來可能很吸引人,而且對於食用高精緻碳水化合物(即糖)飲食的人來說可能是正確的,但沒有證據表明這適用於總碳水化合物含量高而蛋白質含量低(且所有蛋白質均來自植物)的全食物蔬食飲食。幾乎每個採用全食物蔬食飲食的人都會減重,降低血糖和胰島素水平,並解決糖尿病和相關疾病。以植物蛋白為基礎的飲食(如高碳水化合物的全食物蔬食飲食)也會降低總血液膽固醇和導致心臟病的斑塊形成,這些效果在低碳水化合物、以動物蛋白為基礎的飲食中則未見。直接駁斥了陶布斯的預測,全食物蔬食飲食也成功促進體重減輕,而且沒有低碳水化合物飲食伴隨的嚴重副作用。
我先前已總結了低碳水化合物飲食的副作用:更多頭痛、口臭、便秘和肌肉痙攣。與其他沒有這些副作用的飲食策略相比,低碳水化合物飲食幾乎沒有或根本沒有一致的健康益處。而且,即使低碳水化合物飲食確實出現明顯益處——特別是體重減輕——這些益處也無法持久。除了不一致且相對微小之外,所謂的健康益處往往在一年內消失。但更重要的是,低碳水化合物飲食能否顯示任何益處,取決於與其比較的對照飲食。
低碳水化合物飲食「益處」的脈絡
通常,低碳水化合物飲食的評估是透過與標準美國飲食(SAD)進行比較——正如我們所見,SAD被誤導性地標示為「低脂」,而實際上(與脂肪僅佔熱量10%的全食物蔬食飲食相比)它不僅脂肪含量高,動物蛋白含量也高,抗氧化劑和複合碳水化合物含量則偏低。SAD約有30%至40%的熱量來自脂肪。這是巨大的差異!SAD的總蛋白質含量平均也比全食物蔬食飲食建議且能輕易提供的量高出約70%(這意味著約半數美國人的蛋白質攝取量甚至更高)。幾乎所有這些過量蛋白質都來自動物性食物。換句話說:至少90%至95%的美國人食用的是碳水化合物貧乏、相對豐富的飲食,其動物蛋白含量已接近阿金斯飲食法的水平。
由於這種相似性,當阿金斯/陶布斯低碳水化合物飲食與標準美國飲食(SAD)的適度變體進行比較時,任何觀察到的有益效果大多是隨機且相對微不足道的,儘管這並不妨礙低碳水化合物的宣傳高手們盡可能地將其製成頭條新聞。相比之下,真正的飲食比較還應包括全食物蔬食飲食(WFPB diet)——但這種情況幾乎從未發生。
這一點在 Gardner 等人於 2007 年進行的一項研究中表現得再清楚不過了。該研究的目的是比較四種流行飲食在減輕體重方面的能力,他們的特別關注點是調查低脂飲食是否確實能夠減輕體重。因此,我發現尤其令人反感——且顯而易見——的缺陷是他們未能使用真正「低脂」的飲食進行比較:他們將阿金斯飲食和其他幾種飲食的結果與他們聲稱的歐尼斯飲食(一種基於迪恩·歐尼斯博士研究成果的低脂、全植物性食物飲食,歐尼斯博士是利用 WFPB 飲食逆轉心臟病的先驅)進行了比較。
真正的歐尼許飲食,如同全食物蔬食(WFPB)飲食一樣,僅含10%至12%的脂肪。但這篇對阿金斯飲食友好的研究論文的作者,卻使用了一個嚴重扭曲版本的歐尼許飲食,其中含有29%的脂肪,並稱其為「極低脂」!這種扭曲更為嚴重,因為作者們所謂的歐尼許飲食還含有18%的蛋白質,這比植物性飲食中通常含有的蛋白質高出70%至80%。在Gardner等人捏造的歐尼許飲食中,脂肪和蛋白質佔總熱量的48%,而非真正歐尼許計畫中的20%至22%。
用於比較的其他飲食是兩種與標準美國飲食(SAD)非常相似的變體:LEARN飲食和區域飲食(Zone diet)。總體而言,由於這四種營養相似的飲食在膳食脂肪和蛋白質(這兩種衡量標準最能代表這些飲食計畫與真正低脂、低蛋白的全食物蔬食飲食之間的差異)方面的相似性,它們在顯示有意義且具統計顯著性差異的能力方面受到嚴重限制:脂肪和蛋白質分別佔總熱量的65%、54%、51%和48%,這些都遠遠超過全食物蔬食飲食的22%。當然,在研究結束時觀察到了一個科學上隨機的差異:他們發現阿金斯飲食的體重略低於SAD和歐尼許飲食,而這個科學上不顯著的發現卻被當作極其重要的頭條新聞。
由於這項研究註定會引起媒體的廣泛關注,因此在它發表於著名的《美國醫學會期刊》(JAMA)時,就需要進行批判。傳統科學中的批判通常以廣為接受的讀者投書形式進行,這可以被視為同行評審過程的另一個方面。因此,我們四位業內人士適時地向期刊編輯提交了我們的信函,指出該研究的嚴重缺陷並尋求研究人員的回應。通常情況下,這類信函在經過適度的同行評審後會被發表——但在這種情況下卻不然。《美國醫學會期刊》的編輯拒絕了我們所有的四封批判信函,其中包括歐尼許醫生本人的信函,他的飲食正被如此嚴重地歪曲。在我整個職業生涯中,我發表了許多研究論文,並在幾個科學期刊的編輯審查委員會任職,從未見過如此不道德和卑劣的行為。讀者有權聽到我們的批判和研究人員對此的回應,但他們卻什麼也沒聽到。因此,這項研究,如同許多類似的發現一樣,未受質疑,並從此被斷言為證明低碳水化合物飲食優越性的基礎證據。
另一項近期備受矚目的研究也未能納入營養成分差異足夠大的飲食,以致研究人員無法分析和辨別其效果,從而無法在適當的背景下評估和理解不同的飲食。這項發表於《新英格蘭醫學期刊》的研究題為「地中海飲食對心血管疾病的初級預防」,探討了地中海飲食在預防心臟病發作和中風方面的所謂健康益處。其參與者均為心血管疾病高風險族群,但在研究時尚無心血管疾病,他們被隨機分配到三種飲食組之一:「補充特級初榨橄欖油的地中海飲食、補充混合堅果的地中海飲食,或對照組飲食(建議減少膳食脂肪)。」
根據研究人員的說法,他們的發現顯示,兩種版本的地中海飲食——添加橄欖油的和添加堅果的——都比標準的低脂美國飲食更健康。「低脂」組發生了109次「事件」(中風和心臟病發作),而地中海橄欖油組僅為96次,地中海堅果組僅為83次。
乍看之下,您可能會同意那些稱此發現是對抗錯誤低脂飲食之戰的重大打擊的研究人員(以及低碳水化合物的吹噓者)。但深入探究這項研究,卻會發現截然不同的情況。
在我告訴您研究人員報告的實際數字之前,請大膽猜測一下這三種飲食中脂肪的百分比。您可能會認為,被描述為「低脂」的飲食,其脂肪含量應該遠低於那些被吹捧為「低碳水化合物」的飲食,對吧?嗯,那您就錯了。到試驗結束時,兩個地中海飲食組的熱量約有略高於41%來自脂肪,而所謂的「低脂」對照組則有37%的熱量來自脂肪。
總熱量中百分之三十七來自膳食脂肪,竟被視為低脂飲食?百分之四的膳食脂肪消耗量差異,算是顯著差異嗎?
純粹好玩,讓我們將這些結果繪製成圖表,並與標準美國飲食(SAD)和全食物蔬食(WFPB)飲食進行比較:
頭條新聞應該是這樣寫的:「三種幾乎同樣糟糕的飲食,產生幾乎同樣糟糕的健康結果。」
我無法過度強調這種對低脂飲食定義的扭曲有多嚴重,或者這種扭曲在低碳水化合物倡導者發表的科學論文中出現得有多普遍。近期有三篇關於低碳水化合物飲食與其他飲食比較的綜述,分別發表於2003年、2006年和2009年。這些總結相當重複,大多包含相同的研究,其中受試者通常超重至肥胖。每份報告都得出結論,平均而言,低碳水化合物飲食干預通常會導致一些體重減輕和心血管疾病風險指標的有利但可變的變化(這些結論在摘要中被強調,摘要提供了這些研究中大多數外行人會看到的唯一主要信息)。在所有這些文獻中,我們都看到對「低脂」飲食的同樣誤解,以及飲食種類缺乏多樣性的情況一再重複。「低脂」總是約為30%的脂肪(或更高),而不是WFPB飲食的10%至12%脂肪。在這些研究中,對照組飲食和低碳水化合物飲食都富含動物蛋白,而植物性食物含量低,這使得很難看到當比較範圍更廣的營養成分時我們所知道存在的結果。
關於低碳水化合物飲食的完整真相
低碳水化合物飲食的倡導者們,在過去約四十年間,成功地贏得了一大部分市場。部分原因在於,他們傳達的訊息是許多人想聽到的:關於他們壞習慣的好話。
多年來,我發現越來越難以接受低碳水化合物倡導者的滑稽行徑。他們改變了「低脂」飲食定義的基準,並使其看似正常。他們鼓吹攝取大量動物蛋白。他們利用「低碳水化合物」的概念來負面影射碳水化合物的來源:全植物性食物。他們這麼做是為了自身利益:保護甚至擴大高脂肪、動物蛋白為主的食品市場。陶布斯和許多其他低碳水化合物倡導者,利用大量精心挑選但斷章取義的細節,為他們的論點披上科學的外衣,但這些論點在仔細審視下根本站不住腳。請別誤會我的意思:當這些細節被用來描述一個準確的整體時,它們可以而且確實有用。但是,當細節被編織成一個虛假的敘事,以支持一種具有令人不快的副作用和嚴重長期後果的飲食時,就該大聲疾呼,敲響警鐘了。
在描述他們的飲食時,無論是在研究中還是在一般討論中,低碳水化合物倡導者通常將其與我們本已不良的標準美國飲食(SAD)和/或政府推薦的僅略微修改的「低脂」版本進行比較。正如我們所見,這是一種錯誤的比較。我們的飲食,甚至其略微修改的政府認可版本,並非低碳水化合物人士所聲稱的那樣。首先,SAD的總蛋白質含量本已偏高——比理想值高出約70%——而且其中約70%是來自動物性食物的蛋白質(因此限制了植物性食物及其抗氧化劑和複合碳水化合物的攝取)。其次,SAD的脂肪含量是科學建議量的三到四倍。簡而言之,它是一種富含脂肪、富含蛋白質,且通常富含精緻碳水化合物的飲食。這就是低碳水化合物倡導者所謂的「低脂」基準,他們用此來證明其飲食優於所有其他類型的飲食。這些都是非常嚴重的歪曲。
聲稱過去四十年來採用的政府推薦「低脂」飲食只導致更多肥胖,簡直是狂妄自大到了極點。即使美國大眾確實遵循了建議並減少了膳食脂肪(即便如此,最多也只能說膳食脂肪佔總熱量的比例從約35%降至33%),這也不能用來正確評估像全食物蔬食(WFPB)飲食這樣真正低脂飲食(其中只有10%至12%的熱量來自脂肪)的健康益處。
我確信像陶布斯這樣的低碳水化合物倡導者都知道這一切。但是,他們非但沒有讓這點暴露他們論點的尷尬之處,反而試圖輕蔑地將全食物蔬食(WFPB)飲食(例如Gardner等人研究中的歐尼許飲食)描述為「極端」,以此來解釋這些事實。真正的低脂飲食在這些討論中幾乎從未被考慮,即使被考慮,也會被扭曲以使其更像標準美國飲食(SAD)。如此一來,低碳水化合物倡導者巧妙地消除了實驗觀察這些飲食之間真實、攸關生死的差異的可能性。
低碳水化合物倡導者也專注於體重——而非健康。低碳水化合物飲食無法像全食物蔬食(WFPB)飲食那樣逆轉並維持晚期疾病的逆轉。比較不同國家的飲食習慣時,高脂肪、高蛋白飲食(如低碳水化合物飲食)始終與較高的多種癌症、心臟病和其他疾病的發生率相關,而非較低。植物性飲食則顯示相反的效果。事實上,在我所知的數百項研究中,沒有一項研究顯示低碳水化合物(高蛋白、高脂肪、低纖維/複合碳水化合物)飲食與較少的癌症、心臟病或糖尿病相關。
或許關於低碳水化合物飲食與健康最能說明問題的報告,是2013年1月發表的對17項研究(涉及272,216名受試者)的近期總結,其中顯示低碳水化合物飲食導致總死亡率統計學上顯著增加31%。這個發現比統計數據所顯示的更具說服力,因為與全食物、植物性飲食相比,這31%的增加是相對於標準美國飲食(SAD)本已觀察到的高死亡率而言。此外,這項研究是我們首次有機會根據多國長期人口數據來考量低碳水化合物飲食的主張和推論。這些發現,以及低碳水化合物飲食無法逆轉心臟病和第二型糖尿病等嚴重疾病的事實,使得低碳水化合物飲食初期常見的體重減輕變得「無關緊要」,正如該報告作者所指出的那樣。
低碳水化合物倡導者喜歡貶低此類以人群為基礎的研究,因為它們不允許我們確定因果關係。但這種抱怨僅在針對旨在尋找特定、單一營養素或單一化學物質導致疾病的研究時才有效。營養學並非如此運作。當研究旨在尋找廣泛食物類別之間的關聯時——正如這些研究的情況一樣,它們尋找的是源於廣泛營養素類別的廣泛食物類別對廣泛疾病結果的影響——這種駁斥就遠不那麼有效了。
低碳水化合物倡導者唯一值得正面肯定的健康主張,是他們對精緻碳水化合物(精緻麵粉和糖)的警告。但即使如此,他們也主要利用這個警告來試圖闡述一個更大的觀點:所有「碳水化合物」都是壞的。他們發明了「碳水化合物」這個詞,並用它來將所有碳水化合物——所有植物性食物,因為它們是碳水化合物的唯一來源——一概而論。早已證明,精緻碳水化合物——不再處於其天然、整體形式的碳水化合物——會導致健康問題。這並不意味著我們可以利用這個發現來全面抹黑複合碳水化合物,包括纖維和澱粉。
低碳水化合物飲食的論點完全建立在斷章取義、高度還原論的結果之上,這些結果被編織成一幅既不反映科學數據總和,也不反映健康現實的圖景。而那種健康——不僅僅是短期的、不可持續的體重減輕,而是真正的、持久的、充滿活力的健康——無論是對個人、整個社會,還是對地球而言,都是我們都應該追求的目標。
現在是時候將低碳水化合物飲食及其所謂的益處斥為嚴重的騙局了。它只不過是標準美國飲食本已糟糕的營養狀況的延續,而且其方向實際上使我們的個人和集體健康狀況更加惡化。
附錄:舊石器時代飲食法
在前文中,我列舉了幾種低碳水化合物飲食的變體,包括瑪莉·丹和麥可·伊德斯的《蛋白質力量》、貝瑞·希爾斯的《進入區域》、彼得·迪亞達莫的《吃對血型》、亞瑟·阿格斯頓的《南海灘飲食法》,以及艾瑞克·衛斯曼的《新阿金斯飲食法》。但近年來最受關注的版本是《舊石器時代飲食法》。該書於2002年首次出版,由科羅拉多州立大學運動生理學教授羅倫·科代恩撰寫,其強調高蛋白質攝取的核心訊息,如今根據亞馬遜的列表,已有多種版本和形式。其核心訊息,就是低碳水化合物。以全食物、植物性飲食標準來看尤其如此:它允許甚至鼓勵脂肪佔熱量高達30%至50%,蛋白質佔30%至50%的飲食,只留下少量熱量由碳水化合物供應。(與全食物蔬食飲食的脂肪佔8%至12%,蛋白質佔8%至12%相比。)這本「舊石器時代」的書及其模仿者,如果還沒有的話,可能很快就會成為低碳水化合物類型中最受歡迎的競爭者。那麼,我的看法是什麼?
有許多低碳水化合物飲食大師提供飲食建議,但據我所知,科代恩是唯二在經同儕審查的實驗研究文獻中發表過文章的其中一位(另一位是杜克大學的艾瑞克·衛斯曼),我對這種做法深表敬佩。那麼,讓我們從科代恩的研究開始談起。
科代恩的觀點基於對舊石器時代(石器時代)人類高度推測性的飲食習慣,以及他們當代的對應者——現代狩獵採集者——的研究。他認為,可以研究這些現代狩猟採集者的飲食,作為舊石器時代飲食的替代品。然而,他在其研究論文的多處承認,對這兩個人群飲食攝取量的估計都「本質上是主觀的」。他也承認,試圖對來自包含全球862個社會的大量彙編資料中,這些推測攝取量進行評分的「分數並不精確」。此外,他指出,真正的「狩獵採集生活方式」——一種未受西方生活影響的生活方式——「如今可能已經滅絕」。因此,研究人員「必須依賴間接程序來重建農業時代以前人類的傳統飲食。」這是對此研究誠實但略帶歉意的看法。
在2000年之前,人類學家似乎已達成共識,此共識源於理查·李於1968年發表的一篇著作,認為在五十八個不同的狩獵採集社會中,僅約33%的食物來自動物。然而,科代恩在2000年的一篇研究論文中,提出了一個截然不同的估計。與李不同,科代恩將魚類納入其動物性食物的定義中,並增加了更多狩獵採集社會作為其審查對象(229個,而非58個)。科代恩隨後得出結論,這些「舊石器時代」飲食中,66%至75%為動物性食物——此比例至少是李先前估計的兩倍。
透過這種方式擴大研究範圍,科代恩大幅改變了討論的方向。如今,古代飲食習慣不再被視為主要以植物為主,而是被認為以動物為主。科代恩聲稱,他的新估計得到了另一份對較小規模狩獵採集社會進行的「更精確」報告的支持,該報告結論是這些飲食中有65%為動物性食物——非常接近科代恩自己估計的68%。
在其著作中,科代恩熱衷於將人類描繪成相當食肉的動物,暗示「在我們屬的進化早期,人科動物可能經歷了許多類似於貓科等專性食肉動物對動物性飲食的基因適應。」他接著說,「即使在較低的[熱帶]緯度地區全年都有植物性食物來源,動物性食物仍是全球大多數狩獵採集者的首選能量來源」,並且,「野生動物的組織幾乎總是代表著當今世界狩獵採集者的主食。」如同其他低碳水化合物倡導者一樣,科代恩將食用動物性食物視為人類傳統中近乎神聖的一部分,其根源深植於我們遙遠的過去。
科代恩對早期人類飲食的新詮釋,已在科學文獻中受到多方面的挑戰。首先,根據人類學家凱瑟琳·米爾頓的說法,科代恩關於當代狩獵採集者能代表歷史上狩獵採集者的假設,可能有些牽強。大多數早期的狩獵採集者在現代狩獵採集者調查收集之前就已消失或被推向邊緣環境(科代恩也認同此觀點)。因此,這些較近期的狩獵採集者是否是「代表人類原始狀態的倖存者」,值得懷疑。
其次,科代恩提出的挑釁性觀點,即人類「可能經歷了許多類似食肉貓科動物對動物性飲食的基因適應」,實際上只是一種猜測(注意他使用了「可能經歷了」)。據我所知,沒有證據表明有利於食用動物性食物的基因適應,其規模足以將早期人類轉化為真正的食肉動物。
第三,人類無法自行合成維生素C,維生素C僅在植物中製造。其他需要維生素C的哺乳動物都是植食性動物;相比之下,飲食主要為肉食性的哺乳動物則不需要維生素C。人類為何會有所不同?
第四,在早期歷史的大部分時間裡,人類缺乏捕捉和屠宰大型動物以獲取食物的速度和力量,這使得以動物蛋白為主的飲食可能性相當低。(然而,科代恩確實提出了一個相當合理的論點,認為某些史前群體確實經常狩獵動物,這主要取決於獵人在狩獵中所消耗能量後獲得的高能量回報。)
第五,人類的解剖結構與我們現存最近的非人靈長類親屬,如黑猩猩,有很好的可比性,它們過去和現在都主要依賴植物為食。我們擁有相似的腸道解剖結構(單純的酸性胃、小腸、小盲腸和明顯囊袋狀的結腸),而這些近親非人靈長類的飲食中僅含4%至6%的動物性食物,其中大部分是白蟻和螞蟻。(事實上,科代恩在2004年於科羅拉多州丹佛市舉行的一個研討會上——該研討會也邀請我發表演講——提出了對史前人類飲食中肉類含量的非常相似的估計值——3%至5%。)
綜合來看,這些論點足以反駁科代恩關於史前人類飲食以動物性食物為主的相當籠統的主張的可靠性。我無法理解舊石器時代飲食法的愛好者們,為何能根據如此推測性和不確定的證據——且與採用更直接、更可靠研究方法獲得的現代發現如此不符的證據——對自己的觀點如此篤定。以對古人可能食用的食物的粗略估計作為我們今日應如何飲食的主要證據,對我而言幾乎沒有任何意義。使用從當代狩獵採集人群中獲得的證據作為替代,也引發了同樣的不確定性,尤其是當這些當代人群的飲食很可能已與早期時代的飲食大相徑庭。
此外,還需考慮到考古學研究中,關於動物性與植物性食物飲食估計的高度可疑性,因為植物性食物在化石遺骸中幾乎不留痕跡。再者,我們對史前人類的壽命了解多少?他們是否活得夠久,以至於會罹患與飲食相關的老化退化性疾病?那些針對生育年齡之後——也就是無法再傳遞基因之後——健康影響得出結論的進化論論點,並非特別有說服力;如果我們的祖先活得不夠久,無法罹患這些疾病,那麼化石遺骸就不能作為推斷其長期健康的證據。
我同意人類在其演化過程中必定曾攝取過一定量的動物性食物。但我不同意我們應該利用來自遠古歷史的高度可疑證據,來強硬地斷言現今應攝取的蛋白質和脂肪的正確份量,尤其當我們擁有遠為優越的研究方法和實驗手段時。
如同其他低碳水化合物倡導者一樣,科代恩未能解釋或甚至提及與其假說形成鮮明對比的證據,尤其是支持全食物、植物性飲食健康價值的證據。例如,長期以來已經證實,當比較不同人群的飲食與疾病相關性時(如橫斷面研究),富含脂肪和動物蛋白的飲食(如舊石器時代飲食)與較高的心臟病以及乳腺癌、結腸癌和前列腺癌等癌症的發病率有強烈相關性,僅舉幾例。(雖然我提到橫斷面相關性研究,但我並非從這些相關性推斷特定的因果關係;我只是說,這種長期存在且不容置疑的關係——動物性食物與植物性食物的高比例,以各種方式表達——斷然駁斥了舊石器時代/低碳水化合物倡導者的主要論點。)例如,我不知道有任何研究顯示舊石器時代/低碳水化合物飲食與這些及其他相關西方疾病的較低發病率有關。這裡絕對沒有任何迴旋的餘地。
科代恩和其他低碳水化合物倡導者忽略的另一個深遠影響,是人們採用全食物蔬食(WFPB)飲食後迅速觀察到的顯著健康益處。從目前美國飲食(其脂肪和蛋白質含量僅略低於舊石器/低碳水化合物飲食)轉換到全食物蔬食飲食時,健康益處是廣泛的、出乎意料地迅速,且相對沒有副作用。我尚未見到任何證據顯示舊石器/低碳水化合物飲食能做到這一點,這標誌著舊石器/低碳水化合物飲食與全食物蔬食飲食之間一個真正驚人的差異。
一般而言,遵循全食物蔬食(WFPB)飲食時,不僅能預防心臟病、糖尿病、某些癌症(包括肝癌、胰臟癌和黑色素瘤)以及自體免疫疾病等嚴重疾病,更重要的是,可以阻止其進展甚至逆轉(如《救命飲食》中所述)。治療這些疾病的證據已發表於經同儕審查的專業期刊,我相信在不久的將來,這些相同的益處也將在更廣泛的疾病狀況中得到證實。
您可以在《救命飲食》(以及迪恩·歐尼許、考德威爾·埃塞斯廷、約翰·麥克杜格爾、尼爾·巴納德、喬爾·傅爾曼、潘蜜拉·波普爾等許多醫師的暢銷書)中閱讀更多內容,但證據非常一致:當食用全食物蔬食(WFPB)飲食——一種與舊石器時代飲食截然相反的飲食——時,益處很快就會開始顯現,減緩並經常逆轉各種疾病和不適。舊石器/低碳水化合物飲食是否曾被證明能做到這一點?沒有。從未有過。雖然關於全食物蔬食飲食全面影響的更正式、經同儕審查的研究仍有待進行,但實驗、觀察和臨床證據提供了高度的一致性。這類證據遠勝於舊石器時代飲食所能提供的任何理論機制或「考古學」證據。
《整體: rethinking the science of nutrition》預覽
T. 柯林·坎貝爾博士,與霍華德·雅各布森博士合著
緒論
1965年,我的學術生涯看似一片光明。在麻省理工學院擔任四年研究助理後,我安頓在維吉 ParkingLot工大學生物化學與營養學系的新辦公室。終於,我成了一名真正的教授!我的研究計畫再崇高不過了:透過找出如何讓貧困國家的飲食中含有更多優質蛋白質,來終結兒童營養不良的問題。我的研究地點是菲律賓,這得益於美國國務院國際開發署的一筆慷慨資助。
第一個挑戰是找到當地生產、價格低廉的蛋白質來源。(儘管營養不良主要是整體熱量攝取不足的問題,但在1960年代中期,我們認為蛋白質提供的熱量有其特殊性。)第二個挑戰是在全國各地建立一系列自助中心,向母親們展示如何利用該蛋白質來源幫助孩子擺脫營養不良。我和我的團隊選擇了花生,它富含蛋白質且能在多種不同條件下生長。
與此同時,應我系主任查理·恩格爾院長的要求,我正進行另一個計畫。查理獲得了美國農業部的資助,研究黃麴毒素,一種由真菌黃麴黴產生的致癌化學物質,我的工作是盡可能了解這種真菌如何生長,以便我們能防止它在各種食物來源上滋生。這顯然是一項重要的計畫,因為有相當多的證據顯示黃麴黴會導致實驗室大鼠罹患肝癌(當時的主流假設,至今仍是如此,即任何導致大鼠或小鼠罹患癌症的物質,可能也會導致人類罹患癌症)。
我很快發現,黃麴黴污染的主要食物之一竟然是…花生。在那些多年後才顯得驚人的宇宙巧合之一,我發現自己同時在兩個完全不同的背景下研究花生。而當我深入探究這兩個看似無關的問題(菲律賓貧困兒童的蛋白質缺乏症以及黃麴黴的生長條件)時,我的世界開始動搖,並使我質疑我和大多數其他營養科學家賴以建立事業的許多基石假設。
以下是顛覆我的世界觀——最終也顛覆了我的世界——的主要發現:在菲律賓,攝取最高蛋白質飲食的兒童,最有可能罹患肝癌——儘管這些高蛋白飲食的兒童明顯較富裕,並且更容易獲得我們通常與兒童健康相關的所有事物,例如醫療保健和乾淨的水源。
我選擇追隨這個發現所引導的每一個方向。結果,我的職業生涯軌跡轉向了意想不到且令人不安的方向,其中許多細節詳述於我的第一本書《救命飲食》。我最終意識到兩件事:首先,營養是人類健康的總鑰匙。其次,我們大多數人認為的適當營養並非如此。
如果你想一生免於癌症、心臟病和糖尿病的困擾,那力量就在你的手中(以及你的刀叉上)。但可悲的是,醫學院、醫院和政府衛生機構仍然將營養視為在健康中僅扮演次要角色。這也難怪:標準的西方飲食,以及其時髦的「低脂」和「低碳水化合物」表親,實際上是我們大多數疾病的病因,而非解藥。簡而言之,過去半個世紀以來科學界一直在追尋的「奇蹟療法」,結果並非經過數十年卓越而不懈的實驗室工作精心調製的新型神奇藥物,也不是使用雷射和奈米技術的尖端外科工具或技術,更不是能將我們都變成不朽的阿波羅和維納斯的DNA改造。相反地,健康的秘密一直就在我們眼前,以一個簡單甚至可能乏味的詞語呈現:營養。談到我們的健康,事實證明,王牌就是我們每天放入口中的食物。在學習這一切的過程中,我也學到了另一件非常重要的事情:為什麼大多數人先前並不知道這一點。
醫學和科學研究機構非但沒有接受這些發現,反而有系統地加以駁斥甚至壓制。
鮮少有醫療專業人員意識到,我們的食物選擇,其抵禦疾病的效力遠勝於他們開立的藥丸。
鮮少有健康記者報導透過飲食獲得光彩健康和預防疾病的明確好消息。
鮮少有科學家受過宏觀審視的訓練,反而專精於細察單一數據點,而非領悟深具意義的智慧洪流。
而為他們所有人買單並發號施令的,正是製藥業和食品業,它們試圖說服我們,救贖可以在一顆藥丸或由植物碎片和人工成分製成的強化零食中找到。
真相。它是如何被隱瞞的。以及為什麼。這就是本書的全部內容。
為何再寫一本書?
如果你讀過《救命飲食》,那麼這些內容你可能已經聽過一些了。你了解營養的真相,也稍微聽聞過我和其他科學家在努力將此真相公諸於世時所面臨的阻力。
自2005年出版以來,數百萬人閱讀或聽聞過《救命飲食》,並與朋友、鄰居、同事和摯愛分享其見解。我幾乎每天都會收到對全食物、植物性飲食療癒力量的由衷感謝。儘管這些故事個別來看都是軼事,但它們綜合起來的證據份量卻相當可觀。而且,每一個故事都足以彌補那些從我們集體無知中牟利的強大利益集團在我面前設置的麻煩和障礙。
此外,自2005年以來,我的許多同事進行了各種研究,更強有力地顯示了良好飲食對人體各系統的影響。至此,任何否認或輕視全食物、植物性飲食對個人和社會福祉重要性的科學家、醫生、記者或政策制定者,都根本沒有清楚地看待事實。實在有太多確鑿的證據不容再忽視了。
然而,在某些方面,情況幾乎沒有改變。大多數人仍然不知道健康與長壽的關鍵掌握在自己手中。無論是出於惡意,還是更常見的出於無知,西方文化的主流都執意忽略、不相信,甚至在某些情況下積極扭曲我們應該吃什麼的真相——以至於我們很難相信自己這麼多年來一直被欺騙。通常,接受我們被告知的一切,比考慮存在控制、沉默和錯誤資訊陰謀的可能性更容易。而對抗這種看法的唯一方法,就是向你展示它是如何以及為何發生的。
這就是為何這本新書如此必要。《救命飲食》著重於告訴我們全食物、植物性飲食是最健康的人類飲食的證據。《整體》則著重於為何將這些證據公諸於世如此困難——以及為了實現真正的改變,還需要發生什麼。
整體:各部分之總和
本書分為四個部分。
第一部分,提供了更多關於我及他人對全食物、植物性飲食研究的資訊,我對自《救命飲食》出版以來此研究收到的一些最主要批評的反思,以及更多我個人的背景和歷程,作為理解本書哲學思想來源的背景。
第二部分探討了為何這麼多人不僅難以接受,甚至難以注意到這項研究對健康的影響:西方科學與醫學運作其中的心靈囚牢,或稱典範,使得人們無法看見其外的明顯事實。出於許多原因,我們現在運作於一個只在最小細節中尋找真相,卻完全忽略宏觀大局的典範之下。俗語「見樹不見林」貼切地表達了這一點,只是這裡所涉及的遠不止樹木和森林。現代科學如此沉迷於細節,以至於我們見不到形成層和次生韌皮部等等,更遑論森林。著眼於細節本身沒有錯(我大部分研究生涯都在做這件事);問題出在我們開始否認宏觀大局的存在,並固執地堅持我們所見的狹隘現實,一個充滿我們自身偏見和經驗的現實,就是全部的現實。
這種對細枝末節的沉迷,有個花俏的詞叫做「化約論」。而化約論自有其誘人的邏كل輯,以致於在其魔咒下辛勤工作的人們,甚至看不見還有另一種看待世界的方式。對化約論者而言,所有其他世界觀都是不科學、迷信、草率且不值得關注的。所有透過非化約論手段收集的證據——假設研究能首先獲得資助——都會被忽略或壓制。
第三部分探討了這個等式的另一面:那些為了自身利益而追逐財務成功,從而強化並利用這種典範的經濟力量。這些力量完全操縱了公眾關於健康和營養的對話,以符合他們的底線。我們將探討金錢如何透過多種方式影響成千上萬個微小的決定,這些決定累積起來會對你,也就是公眾,聽到(和沒聽到)以及因此相信的關於健康和營養的資訊產生巨大影響。
最後,在第四部分,我們審視此處攸關的一切,以及若想改變現狀,所需為何。
真相屬於我們所有人
我想講述這個故事,因為這是我對你們,對大眾的虧欠。如果你是美國的納稅人,你支付了我在研究、教學和政策制定方面的職業生涯。我認識太多人,包括朋友和家人,他們不必要地承受著病痛,只因為他們不知道我所知道的一切——而他們也是納稅人。你有權知道你的錢買到了什麼,也有權從其發現中受益。
我個人的免責聲明:我對你是否相信我沒有任何經濟利益。我不銷售保健產品、健康研討會或健康指導。我已經七十九歲了,擁有一個漫長而充實的職業生涯,寫這本書並非為了賺錢。當你開始和朋友談論從這本書中學到的東西,並遇到對我和我的動機充滿熱情的輕蔑時(你一定會遇到!),只需想想他們引用的說法的原始來源。問問自己:他們的經濟利益是什麼?他們壓制我在這裡分享的資訊能得到什麼好處?
講述這個故事是一項挑戰。我深知,對許多人而言,僅由植物組成的飲食聽起來像個古怪的想法。但情況開始改變了。這個想法隨著時間的推移越來越壯大。現有的體系是不可持續的。唯一的問題是,我們會在它拖垮我們之前解放自己嗎?還是我們會繼續用那個體系的殘渣污染我們的身體、心靈和地球,直到它在其自身的經濟重負和生物邏輯下崩潰?
在過去的世代,我們的飲食方式似乎是個人私事。我們的食物選擇,無論好壞,似乎對他人的福祉或苦難,更不用說對動物、植物生命以及整個地球的承載能力,都沒有太大影響。但即使那曾經是真的,現在也不再是了。我們個人和集體的飲食,其影響遠遠超出我們的腰圍和血壓讀數。攸關的,正是我們作為一個物種的未來。
選擇權在我們手中。我希望這本書能鼓勵您做出明智的選擇——為了您的健康,為了下一代,也為了整個地球。
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